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THE PSYCHOBIOLOGIC APPROACH

 

 

THE PSYCHOBIOLOGIC APPROACH TO THE DIAGNOSIS OF THE EATING DISORDERS
by Barton J. Blinder, M.D.

The sections to be presented will cover the clinical manifestations of anorexia nervosa, bulimia nervosa, rumination, and pica. The foregoing diagnostic entities have been defined formally as eating disorders in the Diagnostic and Statistical Manual of the American Psychiatric Association beginning with the Third Edition in 1980 and will continue to be so designated in the Fourth Edition to be published in the 1990's. Before describing these disorders with the focus on clinical symptomatology and diagnostic focus and range it is important to establish certain general principles in the approach to the patient with an eating disorder. Increasingly research in the last decade has uncovered the continuity of basic neurophysiologic structure and process underlying the regulation of appetite and eating derived from animal model research extended our understanding and approach to human clinical eating disorders. It is important to make a fundamental distinction between a feeding disturbance (a relatively transient behavior affecting eating which is clearly derived from anxieties and conflicts in relationship or self-appraisal occurring at different epochs of psychosocial development) and an eating disorder (a psychobiologic regression characterized by de-differentiation, interference or distortion of eating manifested by deficits in: a) appetite regulation; b) food selection or preference; and c) consummatory behavior). An eating disorder is likely to be persistent over time with a surrounding context of habitual attitudes and reactive behaviors that ultimate affect the patient's nutritional and general medical status. Individual psychological defenses and family reactions are usually secondary to the loss of control, the threat to competency, and perceived physical danger. Symptoms of the eating disorder may reactivate early conflicts related to dependence, separation individuation, and personal autonomy. Very often the significance of signs and symptoms of the eating disorder depend upon the complexity of the patient's psychological structure and where they are in the progression of their psychological development.

As an example of the foregoing anorexia nervosa with severe restrictive ingestive behavior may occur in preadolescence without the emphasis on body image distortion but rather presenting a clinical picture of malaise, growth retardation, and ritual obsessionality with regard to food avoidance of specific foods. In adolescence the same restrictive eating pattern is accompanied by exquisite sensitivity to unusual body experience and preoccupation with body size and fear of becoming fat, often ritualistic exercise and calisthenics with more complex mental ideas regarding calories and their significance as well as intense adolescent struggles for autonomy and individuality from parental control. In later adult life the same anorectic restrictive eating pattern may be associated with difficulties in the marital situation, infertility from the amenorrhea, social difficulties, and even in more recent research findings, suggestions of problematic nurturance of children. In middle age and later life similar restrictive eating pattern is accompanied by fears of aging and death often associated with a depressive or melancholic clinical disorder, sometimes an association with bereavement from loss of a spouse, and often accompanied by various health preoccupations and peculiarities focused on the "health" qualities of food rather than calories or effects on body size.

An example of some of the basic dimensions that we consider in the study of eating disorders would include the following: Binge eating desire (a subjective sense and desire that may be characterize by a hyperphagic component, carbohydrate or rarely an associated non-nutritive substance desire); binge eating behavior (this usually is characterized by rapid rate of eating with gulping of easily ingested and obtained food, often occurring outside of usual meal times and occasionally in the middle of the night); reactive behaviors (these may include fasting, induced vomiting, ruminatory regurgitation, rumination, laxative and diuretic abuse, and polydypsia); food enjoyment (this is the hedonic and reward component of food intake. Often this component is reduced in eating disturbances with accompanied depression and diminished with the predominance of a compulsive and stereotyped component to eating in the more severe instances of bulimia); food preference (this refers to the psychobiologic foundation of food selection; distortions are seen in the restriction of cuisine and food selections in anorexia nervosa and in the unusual preference for carbohydrates seen in bulimia, in pica preference is predominantly for non-nutritive substances or for singular foods eaten in a repetitive manner); food preoccupation (this refers to the ideational component of the mental preoccupation with food; in anorexia nervosa one sees the dissociation of mental preoccupation with food, which may be intense throughout the day and result in the purchasing, hoarding, cooking and serving of food to others from actual ingestive behavior. The severe binge eating desire of the patient with bulimia nervosa more often than not leads to obligatory binge eating outside of usual meal times); postprandial state (this refers to a sense of fullness and unusual body experiences related to the act of eating both in anorexia nervosa and in bulimia nervosa. The physiological anlage for distorted postprandial phenomena may be related to delay in gastric emptying found in both anorexia nervosa and bulimia nervosa, decreased bowel time, esophagitis, and rumination found in approximately 20% of patients with bulimia nervosa); and associated features (body image preoccupation and distortion, whivh is especially prominent during adolescence and young adulthood; mood variation or overt mood disorder, which may take the form of an associated overt depressive disorder or severe demoralization with a persistent eating disturbance).

It is important to define the dimensions and the extent of the eating disorder. This is often done by behavioral mapping of the subjective and objective experiences and behavior of the patient. It is important to define the acute or chronic status of the eating disorder, the presence or absence of developmental antecedents, the level of psychological developmental achievement, the degree of family integrity, coping style, and resilience. Psychotherapeutic approaches generally involve clarification and confrontation, and support and interpretation to the patient and the family. Our current approaches are primarily rehabilitative in focus, helping the patient achieve a degree of cooperative self-regulation in relationship to eating and food and reasonable understanding of developmental and family conflicts. Frequently there is a need for intensive reconstructive psychotherapy, however, this must be determined on an individual basis.

Detailed psychiatric investigation should be initiated reviewing the developmental history, the critical aspects of the family environment and specific phenomenology of the eating disorder. Assessments of family coping styles, conflicts, and patient's defenses in reaction to the eating disorder should be evaluated for their appropriateness in facilitating a systematic plan that could lead to treatment goals. A thorough developmental history including thorough family and genetic history, careful assessments of associated disorders such as depression, developmental disorders, adolescent behavior or personality disorders, and an assessment by psychological testing emphasizing special research areas where appropriate such as a more careful assessment of the body image and issues such as autonomy and self-control.

Nutritional deficits and consequences should be carefully evaluated and most often measurements such as body composition, laboratory studies, especially involving measures of protein sufficiency such as serum albumin, transferrin, and C3 complement as well as specific nutritional deficiencies should be assessed carefully. Cardiac function should be measured carefully including EKG and holter monitor before exercise of any significant degree is allowed for the patient. If possible some assessment of measures of activity and physical strength should be done since patients lose their self-perceptive objectivity regarding their levels of activity and their actual physical reserve capacity. Often in severe anorexia nervosa 24-hour cortisol levels are extremely elevated easily distinguishing this disorder from Addison's disease among other clinical differential signs such as apparent over activity rather than fatigue and relentless pursuit of thinness as opposed to worry and concern over declining body habitus and strength.

In summary the eating disorders constitute a group of syndromes (anorexia nervosa, bulimia nervosa, pica, and rumination) characterized by a psychobiologic regression leading to disturbances in appetite regulation, food preference, and consummatory behavior often with associated disregulations in mood, activity, self-perception, and neuroendocrine function. Attempts to cope with these disorders often lead to exaggerated ineffective and often destructive psychological defenses for the individual patient and futile reactions by the family.

ANOREXIA NERVOSA

Since 1980, with the formulation of the Diagnostic and Statistical Manual III in psychiatric practice, formal criteria for anorexia nervosa have existed. Currently with the revision of the aforementioned manual the basic definitions involve refusal to maintain body weight over a minimal normal weight for age and height (for instance a weight loss leading to maintenance of body weight 15% below that expected, or failure to make expected weight gain during a period of growth leading to body weight 15% below that expected), intense fear of weight or becoming fat even though underweight, disturbances in the way in which one's body weight, size, or shape is experienced (for instance, the person claims to feel fat even when emaciated, believes that one area of the body is too fat even when obviously underweight), and in females absence of at least three consecutive menstrual cycles when otherwise expected to occur (secondary amenorrhea); a woman is considered to have amenorrhea if menses occurred only following hormone administration.

Patients with anorexia nervosa frequently present with a history of weight fluctuations and shifts in appetite regulation. Often the most dramatic symptom is an abrupt or gradual shift in food selection (cuisine). This occurs in the direction of lower calorie foods and a shift in the absolute number and variety of foods that are eaten. Often this constriction of cuisine is accompanied by a variety of rationalizations for it such as the fear of fat, reduction in calories, vegetarianism, and various food fads. There is a shift in the consummatory pattern (ingested intake style and day and night eating habits). The patient is often seen to eat very slowly and to cut food into small pieces. Often meals are prepared by the patient in an aesthetically pleasing manner and served to others while the patient does not a morsel.

Patients suffer from a number of postprandial complaints such as after eating bloating and a feeling of fullness. Such complaints in recent years have been shown to be objectively related to delayed gastric emptying and slowed bowel motility, most likely on the basis of lowered metabolism, dehydration, and possibly due to disrupted bowel hormonal controls.

Often patients show disturbances of mood in the direction of depression, agitation, and anxiety. Relatives complains of the patient's snappiness and irritability.

In the history obtained from the patient with anorexia nervosa there is often evidence in a small number of patients of an actual history of mild obesity. The later often forms a central core of defense and resistance that aids the patients rationalization for the reduction of food intake and the vigilant maintenance of a thin body habitus. The patient's body mental representation of the body which consists of their mental visualization, self-evaluation, and actual body sensations is markedly distorted. Although difficult to objectively demonstrate patients subjectively feel that they are extremely large and fat even though seen to be emaciated by others. They depreciate themselves in rating the aesthetic value of their body image and they complain of numerous unusual body sensations such as enlarged shoulders, arms, thighs, hips, and abdomen, although these cannot be objectively seen or measured.

There are a number of reactive behaviors such as occasional vomiting of an induced, ruminatory regurgitation, or rumination type (often in the service of reducing calories). Occasionally laxative or diuretic abuse and polydypsia are present also as part of contraweight maneuvers secretly engaged in by the patient patient.

Anorexia nervosa in the past has been characterized as a relentless pursuit of thinness: A fixed idea connected to the pursuit of a prepubescent body habitus taking the female patient away from the intensity and conflicts surrounding the increased body size, growth, and psychological changes of puberty later adolescence, and young adulthood.

Our recent more sophisticated understanding of eating disorders views anorexia nervosa as a restrictive eating disturbance occurring throughout the lifecycle. Clinical cases have been reported as young as age six and into the geriatric age range. Psychological concerns often vary depending upon the stage of development. Thus prepubescent cases are reported with more equal incidence distribution of females to males (75/25%) often accompanied by an obsessional and depressive clinical picture and growth retardation. Female preponderance (95/5%) occurs throughout adolescence and young adulthood with the percentage of males increasing toward the middle age level and in atypical cases predominating in the geriatric age level. Restrictive eating disorder in children tends to occur with a cognitive picture of rejection and avoidance of both solid food and liquid. Often the child has a phobic avoidance of the notion of taking in food and a fear of swallowing or choking. Sometimes this has been based on a traumatic incident preceding the anorexia but often occurs in the nature of an anxiety episode followed by phobic avoidance. Because of the decreased fat percentage in prepubescent children there can often be a precipitous loss of weight and compromise of fluid and electrolyte status necessitating early hospitalization, bedrest, and supportive approaches to nutrition while psychiatric treatment is being initiated.

Also of particular interest both in childhood cases of anorexia nervosa and in the childhood history of adolescent and young adult patients are early shifts in appetite regulation, food finickiness, shifts in food selection, a history of unusual weight fluctuations, and a locus of body image sensitivity such as early injuries or congenital abnormalities. The symptoms of anorexia nervosa are often minimized by the patient. Professional attention usually results from pressure by the family, spouse, school, or employer. First noticed very often is unusual behavior related to food in addition to the restriction of food selection and quantity of food, unusual food related behaviors such as food hoarding, changed food handling, or slowing in rate of eating.

Sometimes the patients seek nutritional knowledge but one is often amazed by the numerous rationalizations for limiting their cuisine including fears of the toxic aspects of food, and a panople of contemporary health concerns. Increased motoric activity amounting to several hours per day of exercise is frequently found (a portion of this genetic activity may be innovatively concealed). The actual type of activity often include walking, stretching, and calisthenics which although intense do not truly represent a high level of kinetic work due to the patient's real weakness and loss of strength due to muscle deterioration. On the surface patients may state that their grades in school continue to be excellent but on careful inquiry one finds that their actual efficiency of studying is reduced and there is a degree of cognitive dulling with the need to put in many more hours of study to obtain the same results obtained previously.

The common core physical symptoms and signs in anorexia nervosa include amenorrhea (usually of more than three months duration), abdominal discomfort and constipation, bradycardia, cold intolerance, agitation and hyperactivity, pervasive sense of lethargy, insomnia, dry skin, brittle hair and nails, and often musculoskeletal pain. Dental abnormalities are often seen with increased caries due to the vulnerability to the teeth caused by decreased salivation seen in restrictive anorexia nervosa. Unusual cases of foot drop, peripheral neuropathy, and a Wernicke Korsakoff-like syndrome have been reported in patients due to possible thiamine deficiency. The thermoregulatory deficit primarily manifested by cold intolerance often is correlated with the rapidity and extent of weight loss and in recent studies has been shown to correlate to some degree with brain atrophy shown by increasing cerebral ventricular size. Breast atrophy and muscle wasting as well as susceptibility to fractures (due to osteoporosis secondary to amenorrhea) especially of the spinal column are not unusual consequences. The skin may be covered by light downey hair (lanugo hair) the significance of which is not clear but may be related to both heat preservation and a shift to prepubertal status in the hypothalamic pituitary hormonal axis. Cardiovascular signs and symptoms such as palpitations, bradycardia, and hypotension are a reflection of cardiac atrophy and alternations in cardiac metabolism resulting in changes in both myoneural transmission and work efficiency of the heart secondary to the malnutrition. Hypokalemia due to vomiting and laxative abuse in some patients may also add to cardiac complications. In recent years increasing numbers of patients have been studied with co-existing diabetes mellitus and anorexia nervosa. These patients are often exceedingly difficult to treat due to the exacerbation of the eating symptoms by the shifts in endocrine and metabolic status related to the diabetes. Conversely up to 30% of diabetic patients may show some type of either restrictive or bulimic eating disturbance which does not reach the level of a clinical disorder.

The clinical picture of anorexia nervosa often presents with a challenge in differential diagnosis and certainly the following conditions should be considered: Hyperthyroidism, hypothyroidism, adrenal insufficiency, hypopituitarism, inflammatory bowel disease, and CNS or occult neoplasm. Hyperthyroid patients may show weight loss and hyperactivity but also have increased food intake, hyperthermia, heat intolerance, and increased serum thyroid hormones. Hypothyroidism mimics anorexia with symptoms of weakness, constipation, bradycardia, hypothermia and cold intolerance. However, hypothyroid patient often show weight gain, hypo activity, and increased serum TSH.

Adrenal insufficiency may cause bradycardia, hypotension, lethargy, decreased oral intake, however it also causes hyperpigmentation, and decreased intertriginous hair (hyperkalemia, low serum cholesterol). Rarely pituitary dysfunction will cause amenorrhea but there will also be a secondary hypothyroidism, adrenal insufficiency, or changes in prolactin if caused by a mass lesion.

Inflammatory bowel disease and other causes of gastrointestinal dysfunction may be clinically similar to some manifestations of eating disorders but may be diagnosed by abnormal diarrhea and by laboratory and clinical indications of inflammation.

Chronic illness such as tuberculosis and malignancies may cause cachexia but these are not accompanied by the desire for thinness and distorted body image and are usually characterized by other specific clinical signs.

The psychological profile of the patient with anorexia nervosa is often characterized by an obsessional rigid quality to ideas concerning not only the restriction of food and perfectionistic aesthenic body image but also a limited range of affective expression in relationships to family and inhibitions in heterosexual development. In preadolescents and children with anorexia nervosa the cognitive framework is often a phobic and avoidant attitude toward the intake of food and fluids accompanied by signs and symptoms of depression and anxiety. In adolescents there is often a rejection of sexuality, perfectionism, rigidity in thoughts, and a pseudoaltruism and over idealism.

Recent historical studies have suggested that some of the early female saints of the Catholic church may have had clinical anorexia nervosa accounting for their propensity for fasting and asceticism. Chlorosis (the "green sickness" described often in young women in the 18th and 19th centuries) may have been in some instances a form of anorexia nervosa accompanied by anemia (iron deficiency), restrictive eating habits, and psychological disturbances (interestingly the "green" designation initially referred to the patient's pubescent and virginal status).

Finally, recent observations of food related behaviors in anorexia nervosa have yielded interesting observations that may help to both define the patient's clinical status and aid in their nutritional rehabilitation. Often the patient's food preferences are restrictive in fat and refined carbohydrates as well as certain complex carbohydrates such as breads, cereals, and protein (red meat). The patient frequently consumes most vegetables and specific fruits in an effort to control weight gain. Often there is an observable increase in the amount of non-caloric condiments which are used to alter the flavor of food, possibly to make it less appealing (cinnamon, mustard, vinegar). In addition there may be an increased desire for diet drinks, coffee, and tea.

The physical experience with food finds the anorectic cutting the food into small pieces, often shifting the food around in order to arrange it in novel patterns on the plate. The patient eats slowly with prolonged chewing time before swallowing. Sometimes there is a preference for small containers of food and often food is "tossed away" to avoid consumption. Although the patient with anorexia nervosa does not usually induce vomiting very often food is spit out of the mouth secretly and discarded and on occasion ruminatory regurgitation and actual mechanical or chemically-induced vomiting does occur.

Clinical research has shown that patients later presenting as normal weight bulimics with a past history of restrictive anorexia nervosa are likely often to have complicated co-diagnostic problems such as current depressive disorder and a more extensive eating disturbance.

BULIMIA NERVOSA

The most recent criteria for bulimia nervosa consist of the following major features: recurrent episodes of binge eating (rapid consumption of a large amount of food in a discrete period of time usually less than two hours); at least three of the following 1) consumption of high calorie easily ingested food during a binge, 2) inconspicuous eating during a binge, 3) termination of such eating episodes by a abdominal pain, sleep, social interruption, or self-induced vomiting, 4) repeated attempts to lose weight by severe restrictive diets, self-induced vomiting, or use of cathartics or diuretics, and 5) frequent weight fluctuations greater than ten pounds because of alternating binges and fasts; awareness that the eating pattern is abnormal and fear of not being able to stop eating voluntarily; depressed mood and self-depreciating thoughts following eating binges; and bulimic episodes not due to anorexia nervosa or any known physical disorder.

The actual syndrome of bulimia nervosa defined a patient who suffers from powerful and intractable urges to over eat and seeks to avoid the fattening effects of food by inducing vomiting or abusing purgatives. Most often the patient has, in addition, a morbid fear of becoming obese. Usually there are a minimal average of two binge eating episodes a week for at least three months. In addition to the use of self-induced vomiting, laxative, or diuretics patients may also engage in reactive strict dieting or fasting and vigorous exercise in order prevent weight gain.

Although this is predominantly a disorder of women in the age of 12 to the mid-20's, often the bulimia nervosa pattern of behavior may persist into early middle age and up to 10% of cases are seen in males. Rarely have instances of bulimia nervosa been reported in childhood although recently a number of atypical cases have been described involving hyperphagic behavior and self-induced vomiting in children predominantly in reaction to parental loss, abandonment, or childhood bereavement.

Over three-quarters of patients with bulimia practice self-induced vomiting and a modal of frequency of binge eating and vomiting episodes is usually ten per week. Close to one-quarter of the patients with bulimia will abuse laxatives on a daily basis, often in amounts several hundred times the suggested recommended daily dose. Other behaviors such as the chewing and spitting out of food, diuretic abuse, occasional use of enemas, purposeful contamination of food, hoarding, and kleptomania with respect to food have also been described.

Bulimic patients have a dietary chaos with fragmentation of their meal schedule, long periods of fasting between meals a virtual absence of consumption of normal meals. Binge episodes occur outside of normal meal times frequently in early mornings, late afternoons, or in the middle of the night. Middle of the night binging may be a pattern with an equal frequency of occurrence in males. There may also a correlation with sleep disturbance and later onset of obesity. Often the patient consumes rapidly large amounts of carbohydrates, sweets, and easily prepared high calorie foods to the point of abdominal distension and discomfort. Although there is no agreed upon criteria, severe binges may be from 2,000-20,000 calories in one sitting.

Dietary chaos, binge eating, and abnormalities in food selection lead to long periods of true anorexia (such as morning anorexia following middle of the night binging), reactive fasting, and a tendency to increased meal size due to the rebound phenomena of prolonged periods of not eating punctuated by the binges. Recently it has been shown that although the patients with bulimia nervosa are usually of normal weight they may experience episodes of increased serum free-fatty acids and ketones which resemble a starvation state. Despite their normal weight and usually high normal body fat percentage, patients with bulimia nervosa present with a number of clinical abnormalities including oligomenorrhea and amenorrhea and specific nutritional deficits such as iron deficiency, hypokalemia resulting from the episodic vomiting, hyperamylasemia (specifically increased serum salivary isoamylase) which may be related to both the binging and vomiting as well as an abnormal cephalic phase of eating.

Patient with bulimia may show metabolic alkalosis, hypochloremia and hypokalemia. Parotid gland swelling appearing as puffy cheeks is usually due to acinar hypertrophy rather than hyperplasia. As a result of the self-induced vomiting by placing the fingers down the throat, patients with bulimia often have erosion on the dorsal surface of the hand usually near the metacarpal phalangeal joint of the second and third digit (Russell's sign). Dental abnormalities are often prominent with dental erosion on the lingual surface of the teeth from the vomiting, as well as periomyolysis and other abnormalities of the teeth and gums. Often when referring for dental examination it is important that the examining dentist be made aware of the bulimic disorder since this is often concealed.

Bulimia should be differentiated from hyperphagia which is defined as an excessive ingestion of food beyond that needed for basic energy requirements. Ingestion in hyperphagia may occupy unusual amounts of time and eating may be obligatory and disrupt normal activity. In contrast bulimia usually occurs surreptiously in defined episodes and is terminated by abdominal pain, guilt, or sleepiness. Hyperphagic conditions may occur in association with central nervous system disorders such as neoplasms, the Klein-Levin Syndrome (a bulimic-like syndrome occurring in adolescents characterized by moderate obesity, lethargy, and hypersomnia), Frohlichs syndrome, Parkinson's Disease, genetic disorders including Prader-Willie Syndrome (deletion of the long arm of chromosome 15), and in associated major psychiatric disorders such as depression, depressive phase of bipolar disorder, seasonal affective disorder, certain phases of schizophrenia, and in reaction to antidepressants and neuroleptics.

Often a typical patient with bulimia has been found to be a single, Caucasian female in her early 20's often well educated and slightly above average weight for height. Results often show these individuals are more vulnerable to anxiety, depression, impulse behavior, mood fluctuation, confused sex role identity, poor self-esteem, and severe food and weight preoccupations in response to a cultural norm of thinness. Patients with bulimia nervosa often have histories in early childhood of either deprivation or over protection. The deprivational histories often lead to conflict surrounding attachment and loss with eating in response to mood sensitivity leading to relief of either depression, anxiety, or loneliness. Bulimic patients who have been over protected or over stimulated as children, often have vivid memories of their childhood conflicts and describe subjectively a feeling during binging of both recapitulating the earlier sense of security and also some degree rebelling against the limitations of what others regard as rational and healthy eating.

Binge eating occurs in individuals when alone, not only due to the opportunistic situation but also subjectively due to the desire to alleviate a dyshoric mood state. The compulsive postprandial regurgitation after a period of time not only serves as a contra weight behavior but also takes on an acquired meaning related to the satisfaction of asserting self-control by "purging" the body of negative feelings. Investigations of the developmental line of eating and the neurobiology of appetite and eating may provide data to further define bulimia as a disorder in a broader psychobiologic context.

There may be an early developmental and neurobiologic linkage between mood regulation, bonding and attachment, and appetite regulation that underlies the particular linkages in the clinical manifestations of bulimia nervosa. Specific food related behaviors in bulimia involve both polyphagic and carbohydrate specific desires during a binge. However, when not in a binge or binge/purge cycle a bulimic patient may eat cereal, cakes, cookies, ice cream, peanut butter, pasta, and potato chips, thus showing a much broader range of calorie rich foods and not demonstrating the restriction of cuisine seen in anorexia nervosa. The bulimic patient often consumes easily purged foods to control weight gain and craves foods that satisfy taste desires usually sweet or salty. Eating rate is increased and often there are large bites of food with a lowered chewing to swallowing ratio. Food hoarding and kleptomania that is food related, occurs quite frequently as well as unusual food related behaviors such as contaminating food in order to avoid eating it, eating and binging of uncooked or unprepared food. When out of control bulimic patients often disrupt daily school and work activities to wander from store to restaurant to store purchasing food, binging, storing food in the car, and regurgitating. One might regard such behavior as "obligatory," to the extent that it preempts or capriciously interrupts important scheduled activities.

Bulimic patients may have a history of sexual abuse in childhood with severe developmental psychopathology resulting in a co-diagnosis of borderline or self-defeating personality disorder. A more chaotic clinical picture may result magnifying the eating disturbance and exaggerating psychological defensiveness and resistences to treatment. One sees very frequently a family history in immediate relatives of alcoholism, depression, and upon careful inquiry one obtains histories of both bulimic and restrictive eating disorder especially in female relatives.

Early developmental history is often reported as unremarkable, however more recently careful studies are being undertaken to look at early maternal nurturant behaviors and styles within the family. It is possible that the influences of parental models of eating peer group influences, and certain cultural pressures may by an important element in shaping the development of feeding and providing antecedent determinants of bulimia nervosa. Diagnostic clarification will enable us to fully understand and classify clinical subtypes of bulimia nervosa. Multiple factors are involved in both the etiology and persistence of the disorder, further studies are needed to evaluate treatment protocols (pharmacologic, individual and group psychotherapy, behavioral interventions, and nutritional approaches) on the basis of long term clinical course.

PICA

Pica is defined as a pathological craving for either a food item or its constituents or substances not commonly regarded as food. The psychiatric diagnostic nomenclature emphasizes repeated non-nutritive ingestion for a period of time which emerges as a habitual mode of response for the patient. We may view pica in a developmental context, such as determining the age level of a patient, their physiologic state, and the level of cognitive and intellectual development and also relate pica to sociocultural and historical patterns that may determine the actual food selections of a people or a region.

Physiologic studies in animals had shown that pica may result from specific nutrient deficiencies or be part of a nutrient specific appetite.

Analogously the same pattern has been inferred in humans. Nutrient deficiencies and medical consequences such as iron deficiency, lead intoxication, growth and cognitive impairment, and intestinal obstruction are frequently associated with idiosyncratic dietary habits. Additionally pica may be seen in the deteriorating phase of certain schizophrenic patients as well as being frequently observed among the mentally retarded and in the developmental chaos of autistic children. The most prominent incidents of pica occurs in association with iron deficiency in a fascinating array of clinical phenomena. Some examples will follow.

A 43-year-old female who developed anemia secondary to menorrhagia began to show the eating of ice (pagophagia) frequently several ice trays of ice cubes per day. Therapy with oral iron abolished the pica within three weeks.

A 53-year-old female who had a partial gastrectomy 15 years prior to evaluation had demonstrated an esophageal web receiving mechanical dilatation to relieve dysphagia. Her hemoglobin was 7. The patient developed craving for tomato seeds which was rather relentless and constituted a good deal of her eating behavior throughout the day. Parental iron treatment abolished the pica.

A 33-year-old female who developed anemia secondary to carcinoma of the ascending colon developed pagophagia (ice cube eating) which was abolished by oral iron and blood transfusions.

A 48-year-old female developed cautopyreiophagia (ingestion of ashes of 15 burnt match books daily). Her hemoglobin was 6.5 grams and her serum iron was 14. This patient had gastrointestinal bleeding due to a lesion in the cecum and adenocarcinoma of the left lobe of the liver. Iron therapy, surgery, and transfusion abolished the pica.

Early cases of pica dealt with pregnant women who ate clay and were mildly anemic. There were problems interpreting the data from these studies since there were often cultural traditions related to fertility and assuring the safe birth of a child. Current explanations of pica center around developmental studies where pica is viewed as possibly a vestigial instinct, psychodynamic theories related to early maternal deprivation and parental conflict, need state hypothesis that purpose a nutritional deficit and homeostatic compensation, sociocultural determinants that involve ethnic traditions and beliefs related to rights of passage, health, and fertility, consequences of erratic reinforcement in a chaotic unstructured environment, and neurobiologic bases of food selection and ingestive behavior data resulting from animal investigations (iron deficiency leading to pagophagia, pica resulting from labrynthine stimulation, and pica and iron deficiency related to decreased dopamine receptor neurotransmission as an etiologic factor in spontaneous pica).

In children factors such maternal deprivation, joint family structure, parental neglect, child beating, impoverished parent-child interaction, and disorganized family structure have been implicated in those children who develop pica in association with anemia in contrast to children with anemia without pica.

It has also been shown that a significant number of children who demonstrated persistent pica later developed alcoholism. Some additional evidence implicated gastrointestinal distress and a type of gastrointestinal "malaise" which persists after the physiologic cause has been removed. In the later situation pica may persist as a result of physiologic conditioning.

In children ages eighteen to thirty-six months old pica may be considered normal with an incidence of greater than 50%. However, persistence of excessive hand to mouth movement as in pica is abnormal in children older than three. In the past there have been a racial association of double the percentage of incidence of pica in black children 1:6 compared with a Caucasian cohort. Pica has been associated with diets that are not only low in iron but also zinc and calcium in comparison to control diets. In the mentally retarded there are changes in incidence of pica with IQ, the use of medication, and manifestations of behavioral and appetite. The majority of patients with pica are moderately under weight. Pica appears to increase as the IQ increases. There is also an increased incidence of pica in patients with CNS congenital anomalies and associated medical problems such as diabetes, deafness, and seizures.

Pica seems to increase in incidence in patients taking neuroleptic which may be related to diminished postsynaptic dopamine receptor changes. In the retarded behavioral problems associated with pica may include stereotyped behavior, hyperactivity, self-abuse, food related abnormal behaviors including eating off the floor and chewing of objects. Pica may also coexist with rumination, hyperphagia, and anorexia.

Geophagia, sociocultural factors and developmental considerations all have been significant in determining the type of pica. Lead poisoning continues to be a hazard in young inner city children residing in homes that remain with lead base paint have an incidence of excessive blood level bordering on 20%. The persistence of hand to mouth movements in young children, especially from age 18 months to three years, results in the ingestion of lead based paint. Lead may also enter the blood stream by inhalation of particulate lead from automobile fumes and from nearby factories which use lead based materials. Greater environmental sensitivity to protection of the population has slowly but definitely reduced the foregoing hazards. Elevated blood levels had multiple effects on cognition (including learning impairment and behavior, diminished attention span and impulsive behavior) when whole blood levels reach 70 dB micrograms per dl an insidious onset of anorexia apathy and poor coordination may occur. Neurologic complications of chronic lead poisoning may present as mental retardation, convulsive disorders, peripheral neuropathy, behavioral disturbance, or any combination thereof. Reduction in exposure is the cornerstone of prevention in a lead intoxication treatment program and active consultation with medical-social service departments is clearly indicated.

Special types of pica and their medical complications include paper pica which may lead to mercury poisoning and a particular group of signs and symptoms with low serum iron and zinc in association with geophagia in Turkish children who may manifest hypogonadism, hepatosplenomegaly, and dwarfism.

Bezoar is derived from the Persian word signifying "antidote." These were concretions from the alimentary canal of animals and were thought to have both medicinal and magical properties. Clinically bezoars can be characterized as tricho (hair), phyto (plants), and gastro- (mineral or chemical substances). Tricho and phyto bezoars account for over 90% of reported clinical cases. Certain occupational situations (painters who swallow shellac, asphalt workers), medical procedures and treatments (contrast radiography and medically prescribed special diets) may predispose to bezoar formation.

A case example might involve a 17-year-old female in whom a hair ball was found to take up almost the entire stomach and gastrostomy was required for removal. Further clinical evaluation might find that this young woman had trichotillomania and trichophagia. Other factors to consider might be psychosocial tension and conflict in the family as well as the possibility of an obsessional or delusional disorder of some type.

Another example might be discovery of a trichobezoar in a young child exhibiting trichophagia along with iron deficiency and possible irritation and hemorrhage of the gastric mucosa. Fecal impaction has been described in two school age children resulting from sand eating. Pica may also result from iron deficiency secondary to celiac disease. Medical complications resulting from pica such as intestinal obstruction, intestinal perforation, dental complications, hyperkalemia associated with geophagia, hypokalemia with anemia and parisitosis must always be considered. For instance a significant number of children with toxocariasis have a history of pica. Younger patients and children with pica should be routinely screened for parasitism and other possibly orally transmitted diseases.

Radiographic findings may assist in diagnosis of pica and an abdominal flat plate may visualize chips of lead paint, radiolucent paint particles of clay or foreign objects. In intestinal perforation pneumoperitoneum may be seen especially after the ingestion of a sharp object. A radiopaque foreign body may be visualized and a barium swallow may be useful in determining whether a large gastric mass is bezoar, leiomyoma or carcinoma. In rare situations maternal pica of lead based material may result in the birth of infant with radiographic findings of congenital lead poisoning.

Parotid hypertrophy occurs frequently with starch eating. As noted above many delusional and psychotic patients should be screened clinically for pica. Kraeplin was one of the first to document an extraordinary array of inedible materials consumed by psychotic patients and felt that this behavior might be a "vegetative" sign of psychosis: "A perversion of the appetite." For instance an interesting syndrome of nicotinism and myocardial infarction was described in a psychotic delusional patient who repeatedly ate tobacco.

The clarification of the role of iron deficiency as an etiologic factor in spontaneous pica is ongoing. Current ideas center around the possibility of a central nervous system neurochemical iron dependent appetite regulation. Investigations, however, have linked decreased brain iron specifically to decreased dopamine 2 receptors and the consequent reduction of several CNS dopamine driven behaviors. This suggests that there may be a role for the linkage of iron depletion to a dopaminergic component in the psychobiology of food selection.

Mechanisms which ensure variety of food selection and avoidance of possibly dangerous or none nutritive foods may be impaired in pica. Pica in man is indeed a complex behavior with multiple determinants ranging from demands of tradition and acquired tastes in the cultural context to presumptive neurobiologic mechanisms (iron deficiency, CNS neurotransmission, physiologic conditioning).

Clinical consequences of pica may have broad epidemiologic implications as in lead intoxication and geophagia in children leading to severe impairment of intellectual and physical development. Acute and chronic medical complications may pose surgical emergencies (intestinal obstruction from bezoars) as well as more subtle encroaching symptoms of parasitosis intoxications and resulting nutritional deficits.

Although pica, as a naturally occurring behavior in animals, has a parent utility in aiding digestion or overcoming nutritional deficit, its presence in man appear to be the result of culturally contrived or pathophysiologic circumstances and any adaptive value remains obscure. The occurrence of pica in pregnancy, mental retardation, schizophrenia, and autism suggests a psychobiologic significance to link a disturbance in food selection to other complex neuroendocrine mediated responses.

Treatment approaches have been primarily preventative, educational, and directed toward modification of the pica behavior itself. Iron repletion has dramatically reversed pica for those patients whose clinically symptoms were more clearly coincident with iron deficiency from nutritional or covert medical causes. Further investigation of pica may clarify the normal psychobiology and developmental progression of food selection.

RUMINATION

Rumination, which is an uncommon disorder may occur from infancy through adulthood, and is derived from the Latin ruminiare "to chew the cud." Merycism derived from the Hellenic is the act of post ingestive regurgitation of food from the stomach back into the mouth followed by chewing and reswallowing. The two terms after often used interchangeably. Rumination is associated with medical complications such as aspiration pneumonia, electrolyte abnormalities and dehydration and is considered in the differential diagnosis of vomiting and failure to thrive in infants and young children.

From latency through adulthood rumination frequently has a benign course. Recently, however, it has been associated with bulimia, anorexia nervosa, and depression. Past studies have described the disorder to lack of emotional responsivity in attunement between mother and child stemming from early maternal depression and anxiety. Medical disorders such as gastroesophageal reflux and hiatal hernia also are present in the population of ruminating children. Applications of formal behavioral therapy techniques such as aversive conditioning has been common in the past decade complimenting the more traditional approaches utilizing a substitute caregiver. It should be noted that in the psychiatric nomenclature rumination is designated as a disorder of infancy.

The infant shows a characteristic position of straining and arching of the back with sucking tongue movements and the gaining of satisfaction with the rumination. Diagnostic criteria include repeated regurgitation without nausea or associated gastrointestinal illness for at least one month following a period of normal functioning usually for three months, weight loss or failure to make expected weight gain occurs often. Irritability is noted between regurgitations and hunger is often inferred by the observer. Although the disorder occurs most frequently after three months of age it has been reported in as young as a three week old infant and in rare occasions in the neonatal intensive care unit. Consequent failure to thrive with malnutrition may produce severe developmental delays. Interestingly, rumination has been described in families over four generations with the theory proposed that children learned to ruminate by imitation of their parents. The course of rumination may depend on the age of the patient and the severity of the complications. Although the infant may manifest hyperphagia, post ingestive regurgitation leads to progressive malnutrition (sham eating).

In the ruminating adolescent bulimia and affect disorder may be present. Rumination in adults has been associated with gastric carcinoma and anemia. More frequent medical complications occur in the retarded often with the mortality rate as high as 12-20%.

 

A possible differential diagnosis of two vomiting syndromes of infancy may contrast nervous vomiting from infantile rumination. Nervous vomiting: the nature of the vomiting is involuntary, visceral, purposeless, with age of onset as early as the newborn. Mothering is attentive but dysynchonic and increases rather than relieves tension. Typical circumstances of nervous vomiting occur during the baby's responsiveness to environmental stimulation and successful management often lessens excessive stimulation alleviating the tension producing quality of the mother-infant interaction.

In contrast infantile rumination often appears voluntary, behaviorally based, a form of self-stimulation and occurs after three months of age. The mother is frequently emotionally distant and one notes little reciprocal interaction and attunement. Typical circumstances of the vomiting occur in the absence of environmental stimulation when the infant is often alone and management frequently involves increasing environmental stimulation with substitute caregivers who satisfy the infant's needs by efficient and empathic mothering with appropriate reciprocity and attunement.

From a psychodevelopmental perspective rumination may be viewed as a type of voluntary self-feeding compensating for an inadequate mother-infant relationship. It may then become a defensive habit pattern with both functional autonomy and a pleasurable self-reinforcing effect. Rumination has occurred in infants with disorders including reflux esophagitis, hiatal hernia, malabsorption and malnutrition, failure to thrive, prematurity, severe bronchopulmonary dysphagia, growth failure, autism, grand mal epilepsy, tuberous sclerosis, heroin withdrawal, barbiturate withdrawal, severe parental object loss, and severe infection. Repetitive self-stimulatory behavior (head banging, body rocking, and genital and anal/fecal play) resistent to maternal interruption has been observed in ruminating infants.

In young children the persistence or appearance of rumination is often preceded by a tendency to rumination in infancy and is characterized by intensity and frequency changes correlated with emotional arousal. In adolescents the appearance of rumination is often associated with anorexia nervosa, bulimia, anxiety, and depressive disorders and iron deficiency. Rumination in adults may be chronic, or the individual episode is postprandial without nausea, effortless, and predominantly involuntarily in appearance. It may appear occur spontaneously after a hastily eaten meal causing embarrassment or may appear seemingly voluntarily and pleasurable. The symptomatic presence of active ruminatory behavior varies from as little as six months in duration to a lifetime. Patients may complain of food returning to the mouth, belching, precordial distress (possibly due to esophagitis), indigestion, halitosis, and excessive dental deterioration.

Interesting cases of rumination have been noted in the past such as using the rumination as a sham eating technique and utilizing ruminatory behavior to eat and dispose of foods contraindicated medically (fatty foods and meat) which have a strong palatability or preference for the patient. As an example a patient with gallbladder disease would regurgitate and extrude fatty foods after enjoying eating them preventing their absorption which might lead to an attack of cholecystitis.

The presence of specific psychiatric disorder in adult ruminators is unclear, however there are reports of associations with anxiety, atypical personality, affective disorder, and neuroaesthenic traits. Although some would see the persistence of ruminatory behavior in adulthood as a relatively benign trait, this is questionable since medical complications such as aspiration, and severe dental complications may occur. There may be a subgroup of normal weight bulimic patients with primary ruminatory behavior which antedates their bulimic symptoms. These patients are more likely to be polyphagic during binge episodes rather than demonstrating the more usual specific carbohydrate preference. Ruminatory behavior shifts to actual regurgitation during adolescences to promote weight control. Such ruminators may not show the pattern of impulsive behavior, affective disturbance, or the family history of alcoholism seen in other patients formally diagnosed as bulimic. There may be, in fact, two adult subgroups of ruminators one group with minimal psychiatric problems and a second group with an associated eating disorder such as anorexia nervosa or bulimia. Since patients are often reticent about their ruminatory illness the diagnosis of psychiatric disturbance may go undetected.

Ruminatory behavior is prevalent in the institutionalized retarded, often from 2-5%. Frequently individuals with pica also exhibit rumination. CNS lesions such a microcephaly, dilated ventricle, cerebral palsy, apnea, an infantile spasms may be associated with ruminatory behavior. Features such as predominant self-abuse and other food related behaviors such as pica, hyperphagia and anorexia, as well as medical complications, have been associated with ruminatory behavior in the retarded. The later patients seem to utilize the rumination in a self-stimulating manner to relieve internal tension states blocked from social release because of marked communication deficits and inability to seek out external stimulation.

Clinical example might include a 10-year-old boy who lost weight and started ruminating following institutionalization and separation from family. Treatment by increasing environmental stimulation abolished the rumination demonstrating that prompt social stimulation and reinforcement may abort or terminate the ruminatory disorder often related to institutional adjustments.

There are a number of theories regarding the etiology of ruminatory disorder. A behavioral focus would see the rumination as a habit pattern which is enhanced by reinforcement such as attention and food, certain conditions may serve to maintain the rumination as an operant behavior. A habitual response characteristic of rumination is suggested by, at times, its seeming voluntary quality, frequent waxing and waning with environmental stress, and extinction in response to a aversive stimuli.

There are a number of lines of evidence linking rumination with mood disturbance (affective disorder). Infants and children with rumination often appear sad and withdrawn. For instance, a ruminating child may develop features of anaclitic depression due to the absence of a satisfactory love object and an attuned and reciprocal interaction with mother. Numerous descriptions have been presented describing the emotional unavailability of a mother to her child because of maternal depression as well as her feelings of rejection toward an unwanted infant. The child may suffer a significant human object loss of the primary caregiver. Thus the infant or child is understimulated with consequent development of a ruminatory disorder.

An animal experimental model of this type of object loss leading to ruminatory behavior has been observed in primates. There is also a subgroup of children for whom human object loss may be a manifest onset condition for the appearance of ruminatory behavior. In fact, a careful review of the literature reveals that human object loss is the most frequent psychosocial onset event associated with rumination. A pleasurable self-stimulating component of ruminatory behavior may serve as a defense against the pain of human object loss. Protest, despair, withdrawal which are generally associated with human object loss may also be developmentally specific clinical features in the symptom context of rumination following such loss.

Maternal mood disorder may lead to both a genetic factor present in the infant and secondarily to deprivational consequences to nurturance due to the mother's depression both contributing to increased risk for the infant for both mood vulnerability and ruminatory disorder. There may be a subgroup of infants and children with rumination who in fact have an affective disturbance, rejection sensitivity, passivity and increased incidence of psychiatric disorder. Ultimately diagnostic procedures for measuring biologic state and trait markers for affective disorders might be useful in further defining the relationship of rumination subgroups to other specific psychiatric disorders.

Prospective followup of ruminators noting whether a greater than normal incidence of affective or other psychiatric disturbance occurs would clarify this linkage. Biological determinants link rumination with gastroesophageal reflux. In infant and child ruminators diminished lower esophageal sphincter pressure has been found. There may be two subgroups of ruminators one with significant gastrointestinal problems such as reflux or hiatal hernia and another with no significant gastrointestinal structural difficulties.

Reflux has been associated with Sandifers Syndrome. This is a disorder of interest to psychiatrists because the patient who displays head cocking (abnormal movements of the head and neck) and unusual postures may be misdiagnosed as having a tic or dystonic disorder. In fact, the abnormal postures occur during gastroesophageal reflux in a child with a hiatal hernia. Often surgical repair of the hernia abolishes reflux terminating the abnormal movements within several days.

In several patients with hiatal hernias and rumination it has been noted that the rumination often terminated after surgical repair of the hiatal hernia. It has been suggested that rumination should be viewed as part of an extended syndrome of the presentation of gastroesophageal reflux. The role neuropeptides (including opioids in rumination) remains to be precisely defined. There may be a role for peptide hormones such as vasoactive intestinal peptide (VIP), CCK, gastrin, and motilin. Opioid containing neurons innervate the circular muscle and it has been shown that an opioid agonist may totally inhibit postingestive rumination in adults which along with other pharmacologic blocking interventions suggests a central or peripheral opioid mechanism in rumination characterized by opioid receptor insensitivity or a reduction in endorphinergic neurotransmission. Studies in sheep have demonstrated ruminant stomach motility to be controlled by opioid inhibitory and stimulating neurotransmission in the central nervous system. A similar opioid mediating system is important in the regulation of attachment and the response of separation distress in mammals. It is possible that the deficiency of attachment and occurrence of separation may diminish endogenous opioid activity and provoke ruminatory behavior in infancy. Rumination and vomiting have been reported during the post natal withdrawal phase in infants born of narcotically addicted mothers.

The etiology of rumination is unclear. Physiologic, psychodynamic, and behavioral theories have been suggested. Rumination is best seen as a psychobiologic disorder in which psychological and physiological abnormalities combine in varying degrees to produce the ruminatory behavior. Rumination may be on a continuum where the patient might have maximal gastrointestinal pathophysiology such as severe reflux with hiatal hernia and minimal psychological concomitants or the converse where the patient might have minimal gastrointestinal pathophysiology or reflux but severe psychopathology or psychosocial stress.

Proponents of biological theories believe that the psychological factors definitely influence rumination. Multiple stresses in children can produce similar symptomatic behaviors. For the child irritability and discomfort may result in feeling overwhelmed, anxious, or depressed or may be manifest as severe reflux with esophagitis. Inferred reflux esophagitis treated either medically or surgically may result in a feeling of well being and a termination of rumination.

Psychodynamically oriented treatment using a substitute caregiver may reduce rumination for two reasons. First, the child receives increased stimulation which aids in trust of an attachment. Second, this additional care is effective because the child is held upright during the period of stimulation diminishing both reflux and esophagitis. The esophagitis which subsides augments lower esophageal sphincter pressure further diminishing reflux. Diminished esophagitis results in reduced psychological tension promoting feelings of well being of both the infant and mother.

Maternal anxiety may promote secondary physiologic changes in a child. For example, a mother feeling overwhelmed by a stressful stimulation or feeling anxious secondary to a child's persistent vomiting and weight loss may exhibit increased motoric tension. This is transmitted to the child who becomes tense and developed a more rapid heart rate. The increased autonomic response may alter neuroendocrine controls producing lower esophageal sphincter relaxation and increased reflux. Thus the tendency of the child to ruminate may be increased by an anxious mother. Psychiatric disorder has been associated with both reflux and esophageal contractility abnormalities. Transmitted maternal stress could result in infant gastroesophageal contractile dysfunction promoting reflux and rumination.

Two biopsychosocial sequences of rumination in an infant may be formulated. One involving the predominance of interactive maternal child psychopathology and the other involving the predominance of gastroesophageal abnormality. A close interrelation occurs between mother and infant with various pathophysiologic and emotional stresses. Diagnosis and treatment based on evaluation of both the psychological state of the mother and the infant's gastrointestinal function is indicated.

In summary rumination is an uncommon disorder occurring from infancy through adult life. Its consists of regurgitating and then reswallowing partially digested food. It may result in considerable morbidity in infants and young children. Adult ruminators may have a benign course with embarrassing involuntary reflux or may have an associated eating disorder such as bulimia or anorexia or a mood disturbance such as depression.

Biologic theories of etiology associate rumination with gastroesophageal reflux, hiatal hernia and delayed gastric emptying. Psychological theories discuss infants who have severe failure to thrive and often appear depressed. Severe disincrinty between mother and infant and maternal psychopathology consisting of anxiety, depression, and inability to adequately nurture the child may be present. Behavioral ideas discuss self-reinforcing aspect of the ruminatory behavior. Finally theories of neuropeptide and opioid regulation cause central and peripheral deficits of endorphenergic neurotransmission and receptor sensitivity. Rumination associated with interactive psychopathology may in fact be an affective disorder variant.

Treatment approaches emphasize pharmacologic or surgical treatment of reflux, psychological treatment of the infant-mother disincrinity (with the use of substitute caregivers), and behavioral treatment at times using aversive stimuli (lemon juice, pepper sauce) or positive social reinforcement in response to the stereotype ruminatory behavior. Since rumination may have a biologically or psychologically predominant context a biopsychosocial theory and sequence are the best approach for diagnosis and treatment. Therefore a multiple disciplinary approach to diagnosis and treatment that uses available treatment modalities is imperative to treatment this disorder comprehensively and effectively.

BIBLIOGRAPHY

1. Blinder BJ, Chaitin BF, Goldstein, R: The Eating Disorders: Medical and Psychological Bases of Diagnoses and Treatment. PMA Publications, New York, 1988, 43 chapters.

2. Blinder BJ, Goodman S, Goldstein R: Rumination in The Eating Disorders, 1988, PMA Publications, New York.

3. Blinder BJ, Goodman S: Pica in The Eating Disorders, 1988, PMA Publications, New York.

4. Sibley D, Blinder BJ: Anorexia Nervosa in The Eating Disorders, 1988, PMA Publications, New York.

5. Goodman S, Blinder BJ: Atypical Eating Disorders in The Eating Disorders, 1988, PMA Publications, New York.

6. Leichner P, Gertler A: Prevalence and Incidence Studies of Anorexia Nervosa in The Eating Disorders, 1988, PMA Publications, New York.

7. Meermann R, Napierski C, Vandereycken W: Experimental Body Image Research in Anorexia Nervosa Patients in The Eating Disorders, 1988, PMA Publications, New York.

8. Gwirtsmann HE, Hohlstein LA, Roy-Byren P: New Neuroendocrine Findings in Anorexia Nevosa and Bulimia in The Eating Disorders, 1988, PMA Publications, New York.

9. Kaye WH, Ebert MH, Lake CR: Disturbances in Brain Neurotransmitter Systems in Anorexia Nervosa: A Review of CSF Studies in The Eating Disorders, 1988, PMA Publications, New York.

10. Hsu LKG: The Etiology of Anorexia Nervosa in The Eating Disorders, 1988, PMA Publications, New York.

11. Pyle RL, Mitchell JE: The Epidemiology of Bulimia in The Eating Disorders, 1988, PMA Publications, New York.

12. Vendereycken W: Anorexia Nervosa in Adults in The Eating Disorders, 1988, PMA Publications, New York.

13. Densmore-John J: Nutritiona Characteristics and Consequences of Anorexia Nervosa and Bulimia in The Eating Disorders, 1988, PMA Publications, New York.

14. Larocca FEF, Goodner SA: Self-Help in Anorexia and Bulimia: Principles of Organization and Practice in The Eating Disorders, 1988, PMA Publications, New York.

 

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