Identify the most frequent co-occuring psychiatric disorders with Eating disorders patients.
Describe the etiology of eating disorders.
Identify patterns of behavior seen in Eating Disorders Patients.
Describe the most effective treatment regimens available today.
Eating is controlled by many factors, including appetite, food availability, family, peer, and cultural practices, and attempts at voluntary control. Dieting to a body weight leaner than needed for health is highly promoted by current fashion trends, sales campaigns for special foods, and in some activities and professions. Eating disorders involve serious disturbances in eating behavior, such as extreme and unhealthy reduction of food intake or severe overeating, as well as feelings of distress or extreme concern about body shape or weight. Researchers are investigating how and why initially voluntary behaviors, such as eating smaller or larger amounts of food than usual, at some point move beyond control in some people and develop into an eating disorder. Studies on the basic biology of appetite control and its alteration by prolonged overeating or starvation have uncovered enormous complexity, but in the long run have the potential to lead to new pharmacological treatments for eating disorders.
Eating disorders are not due to a failure of will or behavior; rather, they are real, treatable medical illnesses in which certain maladaptive patterns of eating take on a life of their own. The main types of eating disorders are anorexia nervosa and bulimia nervosa. A third type, binge-eating disorder, has been suggested but has not yet been approved as a formal psychiatric diagnosis. Eating disorders frequently develop during adolescence or early adulthood, but some reports indicate their onset can occur during childhood or later in adulthood.
Eating disorders frequently co-occur with other psychiatric disorders such as depression, substance abuse, and anxiety disorders. In addition, people who suffer from eating disorders can experience a wide range of physical health complications, including serious heart conditions and kidney failure which may lead to death. Recognition of eating disorders as real and treatable diseases, therefore, is critically important.
Females are much more likely than males to develop an eating disorder. Only an estimated 5 to 15 percent of people with anorexia or bulimia and an estimated 35 percent of those with binge-eating disorder are male.
Etiology of Eating Disorders
Although the etiology of eating disorders is complex, several national studies have clearly defined histories of childhood physical or sexual abuse as predisposing risk factors for developing eating disorders. There is also compelling evidence that genetic predisposition, premature birth, birth trauma and biochemical individuality also play a significant role in the eventual development of an eating disorder.
Both anorexia nervosa and bulimia nervosa are statistically more common among family members than in the general population, and there is a cross-transmission of both conditions, i.e., a family member of someone with anorexia nervosa is more at risk for developing bulimia nervosa than someone with no family history. The same study also shared findings that suggest atypical eating disorders (binge-eating, etc.) also have familial heritability.
Because it is difficult to definitively separate genetics from environment in familial studies, eating disorder studies involving twins have provided important data concerning heritability. Multiple studies have shown the risk for developing either anorexia or bulimia is significantly greater in identical twins than in fraternal twins and these genetic effects emerge only after puberty. In 50-83 percent of bulimia nervosa cases studied, heredity was determined to be a factor. Comorbidity, the association of two or more pathologies, also occurs in those with eating disorders and their family members. In family members with eating disorders there is a 2.0-3.5 times increased occurrence of bipolar or unipolar depression. In another example of comorbidity, a significant 3- to 4-fold higher lifetime risk for substance use disorders occurs in bulimics, relatives of bulimics, or binging anorexics when compared to relatives of anorexics or controls without eating disorders or a family history of eating disorders.
Serotonin regulation has been shown to be a significant factor in eating disorders. Clinical research suggests that alterations in the serotonin system can affect feeding behaviors. Specifically, serotonin increases satiety responses, which are impaired in bulimics. Insulin resistance, which may be present in anorexia and bulimia, impairs the body's ability to produce serotonin from L-tryptophan. Acute dieting and weight loss can cause low levels of plasma L-tryptophan. Compulsive exercising may also be related to changes in serotonin metabolism induced by food restriction. For example, research has shown a reduction of symptoms in compulsive exercisers when given the selective serotonin reuptake inhibitor (SSRI) fluoxetine.
Low levels of serotonin have been reported in low-weight anorexics. The lack of serotonin as a substrate has been suggested as the reason that anorexics do not typically respond to the SSRI-class antidepressant therapies. (23) Not all studies of cerebrospinal fluid (CSF) tryptophan and serotonin levels in anorexics have shown significantly lower serotonin levels, and it remains to be seen whether anorexics without purging behaviors have different serotonin dysfunctions than anorexics with bulimic tendencies.
Bulimia nervosa, in the majority of studies, also appears to be characterized by altered serotonin metabolism. Bulimics have reduced responses to serotonin challenges when given serotonin agonists and low levels of the major serotonin metabolite 5-hydroxyindolacetic acid (5-HIAA), indicating reduced serotonergic activity. Serotonin dysregulation has been implicated in several psychiatric disorders occurring in bulimia and family members of bulimics: substance abuse, alcoholism, major depressive disorder, anxiety, suicidality, and impulsivity.
Binging and vomiting have also been shown to decrease serotonin synthesis, and binge frequency has been inversely correlated with CSF concentrations of serotonin. Even after one or more years in recovery, women with bulimia were found to still have increased core eating-disorder symptoms when compared to healthy controls. They had normal dopamine and norepinephrine levels but increased levels of 5-HIAA, used to assess serotonin levels. Increased 5-HIAA levels after recovery are also found in anorexia. This phenomenon is not well understood and has been described as a possible "rebound" effect of the recovery process.
The Use of Antidepressants, Serotonin Precursors, and Inositol in Eating Disorders
It is well substantiated in the medical literature that those diagnosed with bulimia nervosa respond to antidepressants. However, they are not as effective as cognitive-behavioral therapy and there is little evidence antidepressant therapy alone is effective. It is not known whether the mechanism of antidepressant medication in bulimia is the same as in depression. SSRIs have been shown to be useful only at high dosages (60 mg fluoxetine) in bulimia--higher than are usually used in antidepressant therapy. Also, the presence of diagnosed depression in a bulimic patient is not predictive of whether the antidepressant will be effective for the treatment of bulimia.
Eating disorders are complex conditions that arise from a combination of long-standing behavioral, emotional, psychological, interpersonal, and social factors. Scientists and researchers are still learning about the underlying causes of these emotionally and physically damaging conditions. We do know, however, about some of the general issues that can contribute to the development of eating disorders.
People with eating disorders often use food and the control of food in an attempt to compensate for feelings and emotions that may otherwise seem over-whelming. For some, dieting, bingeing, and purging may begin as a way to cope with painful emotions and to feel in control of one’s life, but ultimately, these behaviors will damage a person’s physical and emotional health, self-esteem, and sense of competence and control.
Psychological Factors that can Contribute to Eating Disorders:
- Feelings of inadequacy or lack of control in life
- Depression, anxiety, anger, or loneliness
Interpersonal Factors that Can Contribute to Eating Disorders:
- Troubled family and personal relationships
- Difficulty expressing emotions and feelings
- History of being teased or ridiculed based on size or weight
- History of physical or sexual abuse
Social Factors that Can Contribute to Eating Disorders:
- Cultural pressures that glorify "thinness" and place value on obtaining the "perfect body"
- Narrow definitions of beauty that include only women and men of specific body weights and shapes
- Cultural norms that value people on the basis of physical appearance and not inner qualities and strengths
Other Factors that can Contribute to Eating Disorders:
Scientists are still researching possible biochemical or biological causes of eating disorders. In some individuals with eating disorders, certain chemicals in the brain that control hunger, appetite, and digestion have been found to be imbalanced. The exact meaning and implications of these imbalances remains under investigation.
Research testing the predictions of cognitive-behavioral theory related to the psychopathology of eating disorders has lagged behind treatment outcome research. Central to cognitive theories of eating disorders is the hypothesis that beliefs and expectancies pertaining to body size and to eating are biased in favor of selectively processing information related to fatness/thinness, dieting, and control of food intake or body weight. In recent years, controlled investigations of the predictions of cognitive theories of eating disorders have yielded empirical support for these theories. This paper reviews research which has tested the predictions of cognitive-behavioral theory and discusses the implications of these findings for the treatment of eating disorders. Understanding of information processing biases may assist the clinician in understanding a range of psychopathological features of anorexia and bulimia nervosa, including denial, resistance to treatment, and misinterpretation of therapeutic interventions. end
An estimated 0.5 to 3.7 percent of females suffer from anorexia nervosa in their lifetime.
Symptoms of anorexia nervosa include:
- Resistance to maintaining body weight at or above a minimally normal weight for age and height
- Intense fear of gaining weight or becoming fat, even though underweight
- Disturbance in the way in which one's body weight or shape is experienced, undue influence of body weight or shape on self-evaluation, or denial of the seriousness of the current low body weight
- Infrequent or absent menstrual periods (in females who have reached puberty)
People with this disorder see themselves as overweight even though they are dangerously thin. The process of eating becomes an obsession. Unusual eating habits develop, such as avoiding food and meals, picking out a few foods and eating these in small quantities, or carefully weighing and portioning food. People with anorexia may repeatedly check their body weight, and many engage in other techniques to control their weight, such as intense and compulsive exercise, or purging by means of vomiting and abuse of laxatives, enemas, and diuretics. Girls with anorexia often experience a delayed onset of their first menstrual period.
The course and outcome of anorexia nervosa vary across individuals: some fully recover after a single episode; some have a fluctuating pattern of weight gain and relapse; and others experience a chronically deteriorating course of illness over many years. The mortality rate among people with anorexia has been estimated at 0.56 percent per year, or approximately 5.6 percent per decade, which is about 12 times higher than the annual death rate due to all causes of death among females ages 15-24 in the general population. The most common causes of death are complications of the disorder, such as cardiac arrest or electrolyte imbalance, and suicide.
Approximately one percent of adolescent girls develop anorexia nervosa, an eating disorder characterized by an irrational fear of weight gain. The condition usually begins around the time of puberty and is associated with restricted eating and extreme weight loss. Anorexia is a mental disorder with significant physical consequences. Affected individuals typically experience an absence of menstrual periods and other health problems which negatively impact bone density.
Anorexia and Bone Loss
Both nutritional and endocrine factors set the stage for bone loss in anorectics. One of the most significant factors is estrogen deprivation. Low body weight causes the body to stop producing estrogen. This disruption in the menstrual cycle, known as amenorrhea, is associated with estrogen levels similar to those found in postmenopausal women. Significant losses in bone density typically occur.
Elevated glucocorticoid levels also contribute to low bone density in anorectics. Sufferers tend to have excessive amounts of the glucocorticoid "cortisol," which is known to trigger bone loss. Other factors, such as a decrease in the production of growth hormone and growth factors, low body weight (apart from estrogen loss), calcium deficiency, and malnutrition have also been proposed as possible causes of bone loss in girls and women with the disorder.
The Scope of the Problem
Bone loss is a well established consequence of anorexia. Recent studies suggest that not only is osteopenia very common, but that it occurs early in the course of the disease. Key studies have found significant decreases in bone density in anorectic adolescents. For example, affected teens have been shown to have spinal density 25% below that of healthy controls. Up to two thirds of teens with the disorder have bone density values more than two standard deviations below the norm.
Studies suggest that half of peak bone density is achieved in adolescence. Anorexia typically develops between mid to late adolescence, a critical period for bone accretion. Affected teens experience decreases in bone density at a time when bone formation should be occurring. Studies have shown that anorectic girls are less likely to reach their peak bone density and are at increased risk for osteoporosis and fracture throughout life.
Anorexia in Men
According to the American Anorexia Bulimia Association, approximately ten percent of eating disorder sufferers are male. While men are much less commonly affected by anorexia than women, research suggests that male victims also experience significant bone loss. A recent study at the University of Iowa found substantial decreases in spinal bone mineral density in anorectic college men. Researchers speculated that weight loss, restricted dietary input and testosterone deficiency may be responsible for the low bone density found in men with the disorder.
Health Consequences of Anorexia Nervosa:
In anorexia nervosa’s cycle of self-starvation, the body is denied the essential nutrients it needs to function normally. Thus, the body is forced to slow down all of its processes to conserve energy, resulting in serious medical consequences.
- Abnormally slow heart rate and low blood pressure, which mean that the heart muscle is changing. The risk for heart failure rises as the heart rate and blood pressure levels sink lower and lower.
- Reduction of bone density (osteoporosis), which results in dry, brittle bones.
- Muscle loss and weakness.
- Severe dehydration, which can result in kidney failure
- Fainting, fatigue, and overall weakness.
- Dry hair and skin; hair loss is common.
- Growth of a downy layer of hair called lanugo all over the body, including the face, in an effort to keep the body warm.
Health Consequences of Bulimia Nervosa:
The recurrent binge-and-purge cycles of bulimia can affect the entire digestive system and can lead to electrolyte and chemical imbalances in the body that affect the heart and other major organ functions.
- Electrolyte imbalances that can lead to irregular heartbeats and possibly heart failure and death.
- Electrolyte imbalance is caused by dehydration and loss of potassium, sodium and chloride from the body as a result of purging behaviors.
- Potential for gastric rupture during periods of bingeing.
- Inflammation and possible rupture of the esophagus from frequent vomiting.
- Tooth decay and staining from stomach acids released during frequent vomiting.
- Chronic irregular bowel movements and constipation as a result of laxative abuse.
- Peptic ulcers and pancreatitis.
Health Consequences of Binge Eating Disorder:
Binge eating disorder often results in many of the same health risks associated with clinical obesity.
- High blood pressure.
- High cholesterol levels.
- Heart disease as a result of elevated triglyceride levels.
- Type II diabetes mellitus.
- Gallbladder disease.
Managing Bone Loss
The aim of medical therapy for anorectic females is weight gain and the return of regular menstrual periods. Research from Children's National Medical Center in Washington D.C. suggests that menses usually resumes when girls have achieved 90% of the standard body weight for their age and height. While calcium intake has not necessarily demonstrated a therapeutic value, a nutritionally sound diet, including adequate calcium and vitamin D, is recommended.
Is Recovery of Bone Loss Possible?
The effect of exercise on bone recovery is not clear. Some studies have identified a skeletal benefit from weight bearing activity in anorectics. However, the potential benefits of exercise need to be weighed against the risk of fracture, delayed weight gain, and exercise induced amenorrhea. The impact of estrogen preparations on bone density in affected girls and young women is also unclear. Estrogen may offer a limited benefit in some patients, but it should not be a substitute for nutritional support.
The longer the duration of anorexia nervosa, the less likely it is that bone mineral density will return to normal. While the possibility for complete recovery of normal bone mineral density is low, weight gain and the resumption of menses increase the likelihood that some gains in bone density will occur. Unfortunately a significant number of girls and young women will suffer a permanent reduction in bone density which places them at risk for osteoporosis and fracture throughout their lifetime.
- An estimated 1.1 percent to 4.2 percent of females have bulimia nervosa in their lifetime. Symptoms of bulimia nervosa include:
- Recurrent episodes of binge eating, characterized by eating an excessive amount of food within a discrete period of time and by a sense of lack of control over eating during the episode
- Recurrent inappropriate compensatory behavior in order to prevent weight gain, such as self-induced vomiting or misuse of laxatives, diuretics, enemas, or other medications (purging); fasting; or excessive exercise
- The binge eating and inappropriate compensatory behaviors both occur, on average, at least twice a week for 3 months
- Self-evaluation is unduly influenced by body shape and weight.
Because purging or other compensatory behavior follows the binge-eating episodes, people with bulimia usually weigh within the normal range for their age and height. However, like individuals with anorexia, they may fear gaining weight, desire to lose weight, and feel intensely dissatisfied with their bodies. People with bulimia often perform the behaviors in secrecy, feeling disgusted and ashamed when they binge, yet relieved once they purge.
Binge Eating Disorders:
Community surveys have estimated that between 2 percent and 5 percent of Americans experience binge-eating disorders in a 6-month period.
Symptoms of binge-eating disorder include:
- Recurrent episodes of binge eating
- characterized by eating an excessive amount of food within a discrete period of time
- lack of control over eating during the episod
The binge-eating episodes are associated with at least 3 of the following: eating much more rapidly than normal; eating until feeling uncomfortably full; eating large amounts of food when not feeling physically hungry; eating alone because of being embarrassed by how much one is eating; feeling disgusted with oneself, depressed, or very guilty after overeating.
- Marked distress about the binge-eating behavior.
- The binge eating occurs, on average, at least 2 days a week for 6 months.
- The binge eating is not associated with the regular use of inappropriate compensatory behaviors (e.g., purging, fasting, excessive exercise).
Binge Eating Disorder: People with binge-eating disorder experience frequent episodes of out-of-control eating, with the same binge-eating symptoms as those with bulimia. The main difference is that individuals with binge-eating disorder do not purge their bodies of excess calories. Therefore, many with the disorder are overweight for their age and height. Feelings of self-disgust and shame associated with this illness can lead to bingeing again, creating a cycle of binge eating.
Eating disorders can be treated and a healthy weight restored. The sooner these disorders are diagnosed and treated, the better the outcomes are likely to be. Because of their complexity, eating disorders require a comprehensive treatment plan involving medical care and monitoring, psychosocial interventions, nutritional counseling and, when appropriate, medication management. At the time of diagnosis, the clinician must determine whether the person is in immediate danger and requires hospitalization.
Treatment of anorexia calls for a specific program that involves three main phases: (1) restoring weight lost to severe dieting and purging; (2) treating psychological disturbances such as distortion of body image, low self-esteem, and interpersonal conflicts; and (3) achieving long-term remission and rehabilitation, or full recovery. Early diagnosis and treatment increases the treatment success rate. Use of psychotropic medication in people with anorexia should be considered only after weight gain has been established. Certain selective serotonin reuptake inhibitors (SSRIs) have been shown to be helpful for weight maintenance and for resolving mood and anxiety symptoms associated with anorexia.
The acute management of severe weight loss is usually provided in an inpatient hospital setting, where feeding plans address the person's medical and nutritional needs. In some cases, intravenous feeding is recommended. Once malnutrition has been corrected and weight gain has begun, psychotherapy (often cognitive-behavioral or interpersonal psychotherapy) can help people with anorexia overcome low self-esteem and address distorted thought and behavior patterns. Families are sometimes included in the therapeutic process.
The primary goal of treatment for bulimia is to reduce or eliminate binge eating and purging behavior. To this end, nutritional rehabilitation, psychosocial intervention, and medication management strategies are often employed. Establishment of a pattern of regular, non-binge meals, improvement of attitudes related to the eating disorder, encouragement of healthy but not excessive exercise, and resolution of co-occurring conditions such as mood or anxiety disorders are among the specific aims of these strategies. Individual psychotherapy (especially cognitive-behavioral or interpersonal psychotherapy), group psychotherapy that uses a cognitive-behavioral approach, and family or marital therapy have been reported to be effective. Psychotropic medications, primarily antidepressants such as the selective serotonin reuptake inhibitors (SSRIs), have been found helpful for people with bulimia, particularly those with significant symptoms of depression or anxiety, or those who have not responded adequately to psychosocial treatment alone. These medications also may help prevent relapse. The treatment goals and strategies for binge-eating disorder are similar to those for bulimia, and studies are currently evaluating the effectiveness of various interventions.
People with eating disorders often do not recognize or admit that they are ill. As a result, they may strongly resist getting and staying in treatment. Family members or other trusted individuals can be helpful in ensuring that the person with an eating disorder receives needed care and rehabilitation. For some people, treatment may be long term.
Research is contributing to advances in the understanding and treatment of eating disorders. Scientists and others continue to investigate the effectiveness of psychosocial interventions, medications, and the combination of these treatments with the goal of improving outcomes for people with eating disorders.
Research on interrupting the binge-eating cycle has shown that once a structured pattern of eating is established, the person experiences less hunger, less deprivation, and a reduction in negative feelings about food and eating. The two factors that increase the likelihood of bingeing—hunger and negative feelings—are reduced, which decreases the frequency of binges.
Several family and twin studies are suggestive of a high inheritability of anorexia and bulimia, and researchers are searching for genes that confer susceptibility to these disorders. Scientists suspect that multiple genes may interact with environmental and other factors to increase the risk of developing these illnesses. Identification of susceptibility genes will permit the development of improved treatments for eating disorders.
Other studies are investigating the neurobiology of emotional and social behavior relevant to eating disorders and the neuroscience of feeding behavior. Scientists have learned that both appetite and energy expenditure are regulated by a highly complex network of nerve cells and molecular messengers called neuropeptides. These and future discoveries will provide potential targets for the development of new pharmacologic treatments for eating disorders.
Further insight is likely to come from studying the role of gonadal steroids. Their relevance to eating disorders is suggested by the clear gender effect in the risk for these disorders, their emergence at puberty or soon after, and the increased risk for eating disorders among girls with early onset of menstruation.
Because fluid loss and fluid restriction are common in eating disorders, electrolyte abnormalities are frequent occurrences. The most serious and frequently documented is potassium loss due to self-induced vomiting, and diuretic or laxative abuse. Hypokalemia can result in cardiac symptoms, specifically arrhythmias and EKG abnormalities. Serum levels are often normal, but intracellular potassium may be low enough to create symptoms. If chronic, it can lead to constipation, skeletal muscle myopathy, and nephropathy. Low magnesium is also common and may be a factor in restoring potassium levels. One study examining 175 eating-disordered individuals found 25 percent had low serum magnesium levels that correlated with muscular weakness, diminished concentration, muscular cramping, paresthesias, arrhythmias, and recent memory loss.
Commonly known as "the refeeding syndrome," phosphate can drop to potentially fatal levels as a result of oral or parenteral refeeding in anorexia nervosa. Hypophosphatemia can also occur as a result of vomiting, excessive exercise, laxative, diuretic, or antacid use (antacids are frequently used in bulimia as self-treatment for reflux esophagitis and gastritis), or binge eating. Low intracellular phosphate levels (serum levels commonly remain normal) usually occur along with low magnesium and potassium levels and can manifest as respiratory distress, signs of pneumonia, cardiomyopathy, skeletal myopathy, and neuropathy. Low phosphate levels during the time of peak bone mass attainment have been correlated with osteoporosis in anorexia nervosa. The high incidence of scoliosis in ballet dancers has also been related to phosphate depletion due to dietary restriction. Phosphorus has been used prophylactically in refeeding of severely underweight patients to prevent hypophosphatemia and its sequelae.
Although serum potassium has been used as a frequent laboratory screening tool for bulimia, urine sodium-to-chloride ratios appear to be the best predictor of bulimic behavior. A ratio of greater than 1.21 was found in 51 percent of bulimic subjects with a five-percent false-positive rate. The same study also found an increased urine anion gap was a significant predictor of bulimia.
Cardiovascular problems occur frequently, particularly in the presence of electrolyte abnormalities. Bradycardia, hypotension, orthostatic hypotension, and symptoms of dizziness and fainting often occur as a result of starvation and dehydration. Sinus arrhythmias are common and do not require intervention, but ventricular arrhythmias are a well-accepted cause of death in eating disorders. Ipecac abuse (in one study 28 percent of bulimics admitted to using this emetic) can cause irreversible cardiac pathologies and fatal cardiomyopathies because it accumulates in cardiac tissue. Chronic purging by either vomiting or diuretic/laxative use can cause hypovolemia that leads to a hyperaldosterone state in an attempt to conserve body fluid. After the cessation of purging, reflex edema may occur that is temporary and benign, although anxiety-provoking in the patient.
Gastrointestinal complications in eating disorders are complex and can be life-threatening. Swollen submandibular glands and parotid glands as well as esophagitis, esophageal spasm, and esophageal tearing and potentially fatal ruptures can occur from constant vomiting. Bulimics may have esophageal disorders that are undiagnosed and contribute to involuntary vomiting. Gastric dilatation may result from binging in either disorder or refeeding in anorexia. Acute pancreatitis can occur as a result of binge eating or in anorexics who are refed. Long-term laxative abuse can cause pancreatic damage and inhibit normal insulin release. Atrophy of the pancreas has been observed in anorexics and, although the size of the pancreas appears to revert to normal with recovery and increases in body weight, it is unknown whether pancreatic function returns to normal. Abnormal motility, reflected in delayed gastric emptying, increased transit time, constipation, loss of peristalsis, irritable bowel syndrome, steatorrhea, and melanosis coli (a dark brown discoloration of the colon secondary to laxative abuse) can have a variety of causes including binge eating, purging, food restriction, laxative abuse, electrolyte deficiency (potassium, magnesium), and dehydration.
Sustained elevations of cortisol have been documented in anorexia in multiple studies, along with proportionately decreased levels of DHEA, DHEA sulfate, and androstenedione. Studies in bulimics have not consistently found elevated cortisol levels. A more recent study, however, did find elevated cortisol and ACTH levels in normal-weight bulimic women. The reason for hypercortisolemia in anorexics is quite simply that starvation increases cortisol output. Studies of even short-term fasting of 2.5 days in midluteal-phase women have shown a 1.7-fold increase in cortisol output over baseline.
Evidence of elevated cortisol in bulimics may reflect their propensity to restrict food intake, a pattern that often leads to binging and purging behavior, or may reflect a biochemical state predisposing them to depression. Increased baseline cortisol as a result of alterations of the hypothalamic-pituitary-adrenal axis (HPA) is a well-replicated finding in the neurobiology of depression. Elevated cortisol, both in plasma and saliva, has been found to be predictive of major depression in both adult females and male and female adolescents and children. Women with a history of childhood abuse and a diagnosis of major depression exhibit exaggerated cortisol responses to stress when compared to healthy women or women with a history of childhood abuse and no diagnosis of major depression. The HPA axis appears to have a reciprocal modulating relationship with serotonin. Serotonin regulation deficits result in hypercortisolemia and may, in part, be responsible for the elevated cortisol levels in underweight anorexics as well as normal-weight bulimics. Clearly, weight gain is necessary for the normalization of the HPA axis in anorexia nervosa. The use of adjunctive therapies to address existing elevated cortisol levels in bulimia is warranted. Studies have not directly addressed the ability of serotonin-directed antidepressants to reduce cortisol levels in bulimia.
Studies addressing the application of phosphatidylserine, a phosphorylated amino acid found in the CNS, that has been shown to lower cortisol levels and improve symptoms of depressive disorders, are warranted in bulimics.
Thyroid function is commonly abnormal in both anorexia and bulimia. The most common laboratory findings are normal thyroxine (T4), normal thyroid stimulating hormone (TSH), and subnormal triiodothyronine (T3), although one study documented low levels of all thyroid hormones in a population of bulimics. These findings correlate with symptoms of fatigue, hypothermia, constipation, bradycardia, and hypercholesterolemia, even if T4 levels are normal. Signs and symptoms of either "sick euthyroid syndrome" (normal T4 and TSH, and decreased T3) or frank hypothyroidism do not necessarily normalize with increased body mass index or remission of binge eating and purging. One study revealed that bulimics, after seven weeks of abstinence, actually had lower levels of free thyroxin, free triiodothyronine, reverse triiodothyronine, and thyroid-binding globulin, than during periods of active binging and vomiting. The authors speculated that binging may have actually raised thyroid hormone levels even though they were still lower compared to controls at the time of active bulimia. There is also some evidence that thyroid atrophy takes place in anorexia.
Blunted or decreased responses to exogenous TSH are common in anorexia, and there was evidence of significant decreases in thyroid volume in a population of 22 anorexics. The authors of this study expressed their concern about the role thyroid atrophy and related symptomology could play in the continuation of both depression and anorexic behavior. Although depression of triiodothyronine and increased production of reverse T3 is an automatic physiological reaction to starvation, the HPA axis may also be involved in eating-disorder thyroid dysfunction. Elevated plasma cortisol was inversely related to the TSH response to exogenous thyrotropin-releasing hormone (TRH) in 16 females with anorexia and low serum total T3 levels.
Hypothalamic-Pituitary-Gonadal Axis and Bone Loss
Amenorrhea is a classic feature of anorexia nervosa and is considered not only to be a result of caloric restriction and weight loss, but also a dysfunction of the hypothalamic-pituitary-gonadal (HPG) system. A variety of factors (HPA axis, thyroid dysfunction, exercise, etc.) alter gonadotropin-releasing hormone pulsing and result in lowered levels of both luteinizing hormone (LH) and follicle-stimulating hormone (FSH). Bulimics are also at risk of HPG dysfunction and may experience irregular menses even if they are normal weight.
Over 50 percent of all patients with anorexia nervosa have evidence of significant osteoporosis and the rate of bone loss appears to be equal to that of menopause, i.e., five percent per year. The consequences are striking. In one study of 27 anorexics followed for 25 months, the relative risk for nonspinal fracture was 7.1 compared to normal women in the same age group. Gains in bone density did not depend on whether the women took calcium or estrogen, regained their menses, attained 80 percent of ideal body weight, or exercised significantly. Even young women who recover before 15 years of age have been shown to have long-term decreased bone density in the lumbar spine and femoral neck. A study examining premenopausal anorexics who had been in recovery for a mean of 21 years still had significantly lower femur bone density measurements than age-matched controls.
Estrogen administration alone has not been shown to prevent progressive bone loss in current diagnosed anorexics and increases in weight alone appear to be insufficient in reversing bone mineral density losses. Bone loss in anorexia has been linked to the metabolic consequences of starvation and weight loss, including metabolic acidosis, hypoestrogenism, malnutrition, elevated cortisol, low insulin levels that may reduce calcium absorption, and decreased hepatic production of insulin-like growth factor-1.
Nutrient Deficiencies Zinc
A significant amount of research has attempted to evaluate the role of zinc in eating disorders. Several symptoms of zinc deficiency, including weight loss, appetite loss, specific forms of dermatitis, amenorrhea, and depression are also commonly seen ill anorexia nervosa. Because zinc deficiency has a wide range of biochemical effects that are seen in eating disorders--alteration of prolactin, thymulin (a zinc-containing thymic hormone), estrogen, cortisol, and the opioid feeding system; lowered testosterone; reduced insulin efficiency; defective insulin-like growth factor-1 signaling pathways; and alterations in serotonin metabolism --there is adequate reason to investigate the potential therapeutic effect of supplemental zinc.
Zinc deficiency also reduces leptin concentrations. Leptin is a peptide produced by adipose cells and affects hypothalamic activity involved in appetite regulation. Leptin receptors are also found in reproductive tissues and low levels of leptin may contribute to reproductive dysfunction. Low levels of leptin are found both in underweight anorexics and normal-weight bulimics. Low leptin in bulimics and anorexics may also contribute to low thyroid hormone levels and abnormalities in the HPG axis found in both eating disorders.
In protein-energy malnutrition, a state that many anorexics achieve, there is a disruption of the small intestinal mucosal absorptive capacity with a resultant decreased capacity for zinc absorption. The acquired zinc deficiency, in turn, perpetuates an altered or "dysfunctional" epithelial barrier and may result in diarrhea, which perpetuates malabsorption.
Diet history and recall studies have found women with anorexia nervosa at high risk for deficiencies of zinc, as well as calcium, vitamin D, folate, vitamin B 12, magnesium, and copper. Evidence of zinc malabsorption also exists in anorexia.
Clinical studies assessing the incidence of zinc deficiency in eating disorders are not all in agreement. Six studies found significantly low plasma, serum, or urine zinc in anorexic patients and two found zinc deficiency in significant numbers of bulimic patients. Three studies found no difference between serum or plasma zinc levels in populations of patients with anorexia nervosa and controls. However, as researchers in the field of zinc nutriture have pointed out, there is currently no universally accepted single measure to assess zinc status in humans, and plasma zinc is considered a poor measure of marginal zinc deficiency.
The need for additional zinc during weight restoration in malnutrition and eating disorders has been evident in several studies. The stated goal of zinc supplementation in anorexia nervosa in clinical trials has been to increase rate of recovery as evidenced by increases in body mass index. In one clinical trial using either 50 mg of zinc gluconate (14 mg elemental zinc) twice daily or placebo, female anorexic patients on zinc were able to achieve a statistically significant increase in rate of weight gain. In an open study of 20 females with anorexia given 45-90 mg of zinc sulfate daily, the authors found 17 had increased their weight by more than 15 percent at follow-up. One patient had a weight gain of 57 percent within 24 months and one patient had a weight gain of 24 percent within three months. None of the study subjects lost weight after starting zinc therapy and 13 experienced the return of their menses within 1-17 months. In other open trials and patient cases the use of zinc supplementation has been shown to improve weight gain.
Zinc supplementation may also benefit psychological as well as growth and developmental parameters in anorexia nervosa. A placebo-controlled study of 15 adolescents, conducted through the Stanford University Pediatrics Department, first looked at evidence of zinc deficiency using 24-hour urinary excretion. The mean zinc loss in the treatment group was significantly lower than the control group. The adolescents with anorexia were then given 50 mg elemental zinc/day for six months. On follow-up, the treatment group had statistically significant improvements in mood and anxiety, in addition to greater weight and height gain, improved taste function, resolution of skin abnormalities, and greater advancement of sexual maturation.
Zinc supplementation has also been studied in bulimia. Forty-seven female bulimic patients were given 120 mL of liquid zinc sulfate for an average of 8.3 days. Patients had significant improvement in both reduction of "fat anxiety" and "weight vigilance" on the Multidimensional Body-Self Relations Questionnaire and the "drive for thinness" and "body dissatisfaction" on the Eating Disorder Inventory (EDI). No information was available concerning changes in frequency of binge-purge episodes or weight changes. In the same article, Schauss also reports favorable outcomes in both anorexia and bulimia with the use of 9.1-18.2 mg daily dosage of elemental zinc in a liquid zinc sulfate form (40-80 mL). That dosage is maintained for 6-15 days or until taste acuity improves according to the zinc taste test and the patient can then switch to an encapsulated zinc supplement.
Thiamine, Riboflavin, Magnesium, and Essential Fatty Acids
Thiamine deficiency has been documented in 38 percent of a sample of 37 anorexics using erythrocyte transketolase activation. Thiamine deficiency has been shown to cause depression, paresthesia, weakness, dizziness, myalgia, palpitations, hypotension, bradycardia at rest, sinus arrhythmias on exertion, cognitive changes, and classic anorexia. It is relevant that individuals with eating disorders are at high risk for abuse of diuretics and alcohol, and often have high simple carbohydrate loads, increasing risk for thiamine deficiency. Wernicke's encephalopathy, a potentially fatal condition if untreated, has been diagnosed in bulimia nervosa.
Riboflavin deficiency in anorexia has been documented in studies of plasma and by erythrocyte glutathione reductase (a riboflavin coenzyme) activity. Riboflavin deficiency due to deficiency of conversion cofactors has also been documented in anorexia. This phenomenon has been hypothesized to be due to low triiodothyronine levels in anorexia nervosa, as T3 is necessary for the production of riboflavin mononucleotide. Because both riboflavin and T3 have been shown to be deficient even after refeeding in anorexics, malabsorption and thyroid replacement even in "sick euthyroid syndrome" should be considered.
Magnesium deficiency has been documented in 25 percent of 175 patients in an inpatient treatment setting. In this group, 19 were normal-weight bulimics, six had restrictive or bulimic anorexia, and 13 had obesity and depression (the remaining patients had thought disorders). Serum magnesium levels below 1.8 mEq/L, when compared to eating-disorder patients with normal serum magnesium levels, correlated with symptoms of muscular weakness and cramping, restlessness, paresthesias, decreased concentration, cardiac arrhythmias, hypertension, and diminished short-term memory. The authors also reported that symptoms occurring in the magnesium-deficient patients improved following either intramuscular or oral magnesium replacement and returned when the oral magnesium supplementation was discontinued. It is important to note that in eight patients with low magnesium levels who had cardiac arrhythmias, magnesium replacement normalized each patient. The cardiac abnormalities included supraventricular tachycardia, atrial fibrillation, and EKG changes, including S-T segment depression, widening of QRS interval with peaked T waves, prolonging of the P-R interval, and S-T segment depression.
Dietary restrictions in anorexia nervosa often exclude sources of dietary fat. Essential fatty acid deficiencies have been found in anorexia nervosa. An assessment of eight patients with anorexia nervosa found polyunsaturated fatty acid deficiencies in plasma phospholipids that were, however, more complex than simple essential fatty acid deficiencies. The implications of this type of aberration are not clear, but the authors stated that anorexia affects the fluidity of plasma phospholipids to a similar extent as is seen in cirrhosis and Crohn's disease.
Winston et al, and Hoffman et al, suggest routine screening be done for thiamine and magnesium deficiency in eating-disordered patients, or, more cost-effectively, thiamine and magnesium supplementation be routinely given to all anorexics. In the same manner, it would be logical to suggest nutrient repletion for the nutrients that have been found to be deficient in anorexics: potassium, phosphorus, magnesium, zinc, thiamine, and riboflavin. Other nutrient deficiencies that have been assessed in the diets of women with anorexia nervosa--calcium, folate, vitamin B1, B2, B12, and copper--may also need to be addressed.
Anorexia nervosa - Anorexia can slow the heart rate and lower blood pressure, increasing the chance of heart failure. Those who use drugs to stimulate vomiting, bowel movements, or urination are also at high risk for heart failure. Starvation can also lead to heart failure, as well as damage the brain. Anorexia may also cause hair and nails to grow brittle. Skin may dry out, become yellow, and develop a covering of soft hair called lanugo. Mild anemia, swollen joints, reduced muscle mass, and light-headedness also commonly occur as a consequence of this eating disorder. Severe cases of anorexia can lead to brittle bones that break easily as a result of calcium loss.
Bulimia nervosa - The acid in vomit can wear down the outer layer of the teeth, inflame and damage the esophagus (a tube in the throat through which food passes to the stomach), and enlarge the glands near the cheeks (giving the appearance of swollen cheeks). Damage to the stomach can also occur from frequent vomiting. Irregular heartbeats, heart failure, and death can occur from chemical imbalances and the loss of important minerals such as potassium. Peptic ulcers, pancreatitis (inflammation of the pancreas, which is a large gland that aids digestion), and long-term constipation are also consequences of bulimia.
Binge-eating disorder - Binge-eating disorder can cause high blood pressure and high cholesterol levels. Other effects of binge-eating disorder include fatigue, joint pain, Type II diabetes, gallbladder disease, and heart disease.
What is required for a formal diagnosis of an eating disorder?
Anorexia nervosa - Weighs at least 15 percent below what is considered normal for others of the same height and age; misses at least three consecutive menstrual cycles (if a female of childbearing age); has an intense fear of gaining weight; refuses to maintain the minimal normal body weight; and believes he or she is overweight though in reality is dangerously thin.
DSM-IV Diagnostic Criteria for Anorexia Nervosa
1. Weight loss at least 15 percent below normal for age/height or failure to make expected weight gain during growth period, leading to body weight less than 85 percent of expected.
2. Weight loss is self-induced by avoidance of high caloric foods, self-perception of body weight or shape as being too fat or big, and intense fear of gaining weight with denial of the seriousness of current low body weight.
3. In postmenarcheal females, amenorrhea defined by the absence of at least three consecutive menstrual cycles. (Amenorrhea is also considered if menses only occur following hormone administration). In males, the disorder, also involving the hypothalamic-pituitary gonadal axis, manifests as loss of sexual interest and potency.
1. Restricting type: absence of binge-eating or purging behavior during current episode of anorexia nervosa.
2. Binge-eating/purging type: regular binge-eating and purging behavior during current episode of anorexia nervosa.
ICD-10 and DSM-IV Diagnostic Criteria for Bulimia Nervosa
1. Recurrent episodes of overeating in a discreet period of time (example: within any two-hour period) at least twice a week over a period of three months.
2. A sense of loss of control during the episode accompanied by a strong desire or sense of compulsion to eat.
3. Recurrent, inappropriate compensatory behavior following bingeing to prevent weight gain: periods of food restriction, self-induced vomiting, laxative misuse or use of diuretics, enemas, appetite suppressants, thyroid preparations or other medications to prevent weight gain. Diabetics who have bulimia may choose to neglect their insulin treatment.
4. Self-perception of being overweight and morbid fear of becoming fat.
5. Behavior does not occur exclusively during episodes of anorexia
1. Purging type: engages in self-induced vomiting or misuse of laxatives, diuretics, etc.
2. Nonpurging type: fasting or excessive exercise are the only compensatory behaviors.
Atypical Eating Disorders
1. Atypical anorexia: key symptoms are present but patient doesn't meet all criteria (menstruates or doesn't have significant weight loss). Patients with physical illnesses that result in weight loss do not qualify.
2. Atypical bulimia nervosa: all of criteria are met except frequency or duration of episodes (less than twice a week or less than three-month duration).
3. Inappropriate compensatory behavior in an individual of normal body weight after eating normal amounts of food (example: self-induced vomiting after eating a normal meal).
4. Binge-eating disorder: recurrent binge eating in the absence of compensatory behaviors like those of bulimia nervosa.
5. Repeatedly chewing and spitting out large amounts of food without swallowing
Bulimia nervosa - At least two binge/purge cycles a week, on average, for at least 3 months; lacks control over his or her eating behavior; and seems obsessed with his or her body shape and weight.
Binge-eating disorder - At least two binge-eating episodes a week, on average, for 6 months; and lacks control over his or her eating behavior.
How are eating disorders treated?
Anorexia nervosa - The first goal for the treatment of anorexia is to ensure the person's physical health, which involves restoring a healthy weight. Reaching this goal may require hospitalization. Once a person's physical condition is stable, treatment usually involves individual psychotherapy and family therapy during which parents help their child learn to eat again and maintain healthy eating habits on his or her own. Behavioral therapy also has been effective for helping a person return to healthy eating habits. Supportive group therapy may follow, and self-help groups within communities may provide ongoing support.
Bulimia nervosa - Unless malnutrition is severe, any substance abuse problems that may be present at the time the eating disorder is diagnosed are usually treated first. The next goal of treatment is to reduce or eliminate the person's binge eating and purging behavior. Behavioral therapy has proven effective in achieving this goal. Psychotherapy has proven effective in helping to prevent the eating disorder from recurring and in addressing issues that led to the disorder. Studies have also found that Prozac, an antidepressant, may help people who do not respond to psychotherapy. As with anorexia, family therapy is also recommended.
Binge-eating disorder - The goals and strategies for treating binge-eating disorder are similar to those for bulimia. Binge-eating disorder was recognized only recently as an eating disorder, and research is under way to study the effectiveness of different interventions
What is Eating Disorders Prevention?
Prevention is any systematic attempt to change the circumstances that promote initiate, sustain, or intensify problems like eating disorders.
Primary prevention refers to programs or efforts that are designed to prevent the occurrence of eating disorders before they begin. Primary prevention is intended to help promote healthy development. Secondary prevention (sometimes called "targeted prevention") refers to programs or efforts that are designed to promote the early identification of an eating disorder---to recognize and treat an eating disorder before it spirals out of control. The earlier an eating disorder is discovered and addressed, the better the chance for recovery.
Basic Principles for the Prevention of Eating Disorders
Eating disorders are serious and complex problems. We need to be careful to avoid thinking of them in simplistic terms, like "anorexia is just a plea for attention," or "bulimia is just an addiction to food." Eating disorders arise from a variety of physical, emotional, social, and familial issues, all of which need to be addressed for effective prevention and treatment.
Eating disorders are not just a "female problem" or "something for the girls." Males who are preoccupied with shape and weight can also develop eating disorders as well as dangerous shape control practices like steroid use. In addition, males play an important role in prevention. The objectification and other forms of mistreatment of women by others contribute directly to two underlying features of an eating disorder: obsession with appearance and shame about ones body.
Prevention efforts will fail, or worse, inadvertently encourage disordered eating, if they concentrate solely on warning the public about the signs, symptoms, and dangers of eating disorders. Effective prevention programs must also address:
- Our cultural obsession with slenderness as a physical, psychological, and moral issue.
- The roles of men and women in our society.
- The development of ones self-esteem and self-respect in a variety of areas (school, work, community service, hobbies) that transcend physical appearance.
- Whenever possible, prevention programs for schools, community organizations, etc., should be coordinated with opportunities for participants to speak confidentially with a trained professional with expertise in the field of eating disorders, and, when appropriate, receive referrals to sources of competent, specialized care.
Author: U.S. Department of Health and Human Services
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