Introduction

Eating disorders are among the most common psychiatric disorders affecting young women.[1] Most notably, anorexia nervosa and bulimia nervosa are significant causes of morbidity and mortality among adolescent and adult females. Because many of these women suffer in silence, the diagnosis of eating disorders can be elusive, and more than half of all cases go undetected.[2] These conditions are associated with serious medical and psychological consequences, including death, depression, osteoporosis, developmental and growth delay, and family disruption. A Finnish study determined that reproductive outcomes are adversely compromised with lower pregnancy and childbirth rates noted in women with eating disorders compared to controls.[3] Early detection and prompt treatment are essential for improving outcomes in what can become a chronic and debilitating condition.[4] Simple screening questions and key physical findings such as low body mass index (BMI), amenorrhea, bradycardia, gastrointestinal disturbances, changes in skin and dentition can lead to the detection of eating disorders.

Gynecologists and other women’s health providers are in ideal positions to screen for these problems and be part of a multidisciplinary team; menstrual cycle irregularities, osteoporosis, infertility, and pregnancy related risk factors are all affected by eating disorders.

The American Psychiatric Association’s Diagnostic and Statistical Manual, Fifth Edition (DSM-5), identifies the feeding and eating disorders listed in Table 38-1.[5]

The principal eating disorders that will be discussed in this chapter are anorexia nervosa, bulimia nervosa, and binge-eating disorder. The core features of both anorexia nervosa and bulimia nervosa are preoccupation with weight gain and excessive self-evaluation of body weight and shape. These disorders occur 10–20 times more often in females than males, especially females aged 15 to 24.[6] It is estimated that 4% of adolescent girls have an eating disorder of which 0.3% have anorexia nervosa. Anorexia nervosa peaks at age 17 to 18 years old. Bulimia nervosa typically has a later onset but is more prevalent than anorexia nervosa.[7] The lifetime prevalence rate of anorexia nervosa has been estimated to be between 0.5% and 3.7%.[8] These entities are psychiatric disorders that have physical complications. Anorexia nervosa has the highest mortality rate of any of the psychiatric diagnoses; the patients die from suicide or a complication of the eating disorder such as an arrhythmia.[9] Therefore, initiation of therapy is essential to facilitate a reduction in associated health risks to the gynecologic patient.

Anorexia nervosa

The three core essential features of anorexia nervosa are:

Anorexia nervosa characteristics are described in Table 38-2. Psychological and behavioral signs and symptoms that are associated with anorexia nervosa are listed in Table 38-3.

The individual with anorexia nervosa maintains a significantly low body weight defined as a weight that is less than that set at a minimally normal level for age, sex, developmental trajectory, and physical health. For adults, the Centers for Disease Control and Prevention (CDC) and the World Health Organization (WHO) have set the lower limit of normal body weight as a BMI of 18.5 kg/m².

The BMI percentiles used to determine level of current severity are as follows:

Anorexia nervosa has two subtypes: restricting type and binge-eating/purging type. Individuals with the restricting type have not engaged in recurrent binge or purging behavior for the past three months with weight loss accomplished primarily through fasting, dieting, and/or excessive exercise. On the other hand, the binge-eating/purging subtype has engaged in recurrent episodes binge-eating or purging (i.e., self-induced vomiting or the misuse of laxatives, diuretics, or enemas) during the past three months.

Bulimia nervosa

Core essential features of bulimia nervosa are:

Inappropriate compensatory behaviors to prevent weight gain include self-induced vomiting; misuse of laxatives, diuretics, or other medications; fasting; or an excessive amount of exercise.

As defined in the DSM-5, an episode of binge eating is characterized by both of the following: (1) the individual eats in a discrete period of time, usually less than two hours, an amount of food that is definitely larger than what most individuals would consume in a similar period of time under similar circumstance; (2) the individual senses a lack of control over eating during the episode. An indicator of loss of control is characterized by the inability to refrain from eating or to stop once the binge has started. A single episode of binge eating is not restricted to one setting. For example, it can begin in one location and continue to another.

The minimum level of severity is based on the frequency of inappropriate compensatory behaviors per week.

Individuals with bulimia nervosa place undue importance on body shape or weight in their self-evaluation. Individuals with this disorder share some resemblance to anorexia nervosa by their fear of gaining weight, a desire to lose weight, or in their level of dissatisfaction with their appearance. However, adult individuals with bulimia nervosa typically are within the range with a BMI ≥18.5 kg/m²–30 kg/m². Bulimia nervosa can occur, although uncommon, in obese individuals. Bulimic individuals typically restrict their diet to low-calorie foods and avoid foods that they perceive as fattening or that trigger a binge.

Bulimia nervosa characteristics are described in Table 38-4.

Binge-eating disorder

The essential feature of a binge-eating disorder is recurrent episodes of binge eating. Each episode is characterized by consuming an amount of food within two hours that exceeds a normal amount that is usually consumed in a similar time period under similar circumstances. A binge-eating episode is associated with at least three of the following:

Additionally, the affected individual demonstrates marked distress regarding the presence of binge eating. The binge eating occurs on average at least once a week for three months. As opposed to bulimia nervosa, the binge eating is not associated with a recurrent use of an inappropriate compensatory behavior. The frequency of binge eating episodes determines the level of security.

Binge-eating disorder occurs in normal-weight, overweight, and obese individuals. The disorder is characterized by individuals consuming more calories and has greater functional impairment, more subjective distress, and psychiatric comorbidity than obese individuals who do not engage in recurrent binge eating.

Common comorbid disorders include depression, anxiety, and bipolar disorders and to a lesser extent substance abuse. Overvaluation of body weight and shape are higher in obese individuals with the disorder than those without the disorder. The psychiatric component is linked to the severity of binge eating and not the degree of obesity. Remission rates and successful treatment outcomes are higher for individuals with the binge-eating disorder. Crossover from binge-eating disorder to other eating disorders is generally not felt to be common,[5] but in one study, crossover from binge eating to bulimia nervosa was high.[10]

Epidemiology

The estimated lifetime prevalence of anorexia nervosa in women is 0.4%, whereas bulimia nervosa is nearly 1.5% and binge eating is estimated to be 1.6%.[5]

Data from the National Comorbidity Replication Survey indicated the median age of onset is 12–13 years old. Teenagers reported significant rates of comorbidity, as well as mental impairment and suicidal ideation.[11]

Predisposed individuals may initially engage in eating disorder behaviors at times of profound body changes, such as those associated with puberty and pregnancy, or of significant life change, such as moving away or starting college. Subtle criticism of weight by parents, peers, boyfriends, coaches, or teachers also can trigger the onset of an eating disorder in a susceptible individual.

Although many are initiated by dieting behavior, eating disorders become self-sustained because they are related to a desperate need for control when life is out of harmony.

Pathogenesis

The most potent risk factor for developing an eating disorder is female gender. The degree of association that is attributed to biological versus social factors is not clear. Twin and family studies indicate that anorexia nervosa, bulimia nervosa, and binge-eating disorder are complex genetic diseases, and each disorder has an estimated heritability range between 50% and 83%.[12–14] A study of 133 families with at least one bulimia nervosa proband provided evidence of significant linkage on chromosome 10p.[15] Additionally, a linkage analysis study of 192 families with anorexia nervosa suggested evidence for the presence of an anorexia nervosa susceptibility locus on chromosome 1p.[16]

Recent MRI studies demonstrated an increased gray matter volume of the medial orbitofrontal cortex (gyrus rectus) in women with restrictive-type anorexia nervosa and those with bulimia nervosa.[17] Orbitofrontal cortex function is associated with a value attributed to food stimuli and to food avoidance.[18, 19] It has been postulated that a larger gyrus rectus in eating disorders is associated with stronger sensory experience of food stimuli, which may be experienced as overwhelming; this then triggers food avoidance.[18, 20] The underlying cause for an increased gyrus rectus volume is unclear. Analyses also indicated other morphologic differences.

The antero-ventral insula gray matter volume was increased on the right side in anorexia nervosa and on the left side in the bulimia nervosa group compared to the control group. The right anterior insula has been recognized in being associated with self -recognition and interoceptive awareness.[21, 22] The fixed perception of being fat while severely underweight in anorexia nervosa could theoretically be related to the right-sided increased anterior ventral insula volume and dysfunction.[23] But, activation of the left anterior ventral insula is related to gastric distention and self-reported fullness.[24] Therefore, an altered anterior insula interferes with the normal interoception in bulimia nervosa, which contributes to a reduced ability to sense satiation and trigger the urge to purge after excessive food intake and the guilt experienced over eating. To summarize, both anorexia nervosa and bulimia nervosa have altered gray matter volume in the gyrus rectus that may be a trait – related structural abnormality.

Another biologic risk factor that has been shown to put female offspring at a higher risk for bulimia nervosa is that of in utero exposure to excessive androgen. Fetal exposure to androgen excess has been attributed to the subsequent development of polycystic ovarian syndrome which is a highly comorbid condition with binge eating and bulimia nervosa.[25] Eating disorders are not of the individual’s own free will, although dieting often precedes it. For some vulnerable individuals, the weight loss originated in an attempt to improve performance or at the suggestion of a coach, but unfortunately, the behaviors became compulsive or excessive. That individual is then caught up in this dilemma and spirals out of control.

Medical complications

Eating disorders have been shown to adversely affect every organ system of the human body. The numerous medical complications of anorexia nervosa are a direct result of caloric restriction and weight loss. Starvation causes protein and fat catabolism that leads to decreased cellular volume and atrophic changes of the heart, brain, liver, intestines, kidneys, and muscles. Some of these complications are reversible with weight gain, but bone mineral density loss is not totally reversed.[26]

Purging leads to most medical complications identified in the patient with bulimia nervosa.

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