Feeding and Eating Disorders

Debra K. Katzman

Neville H. Golden

The focus of this chapter is on feeding and eating disorders in adolescents and young adults (AYAs). Feeding and Eating Disorders in the 5th edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5) include several changes to better represent the disturbances in eating throughout the lifespan.¹ In the DSM-5, feeding disorders of early infancy and childhood, pica, and rumination have been combined with eating disorders in a new section called Feeding and Eating Disorders. The diagnostic classifications in this section include (1) anorexia nervosa (AN), (2) bulimia nervosa (BN), (3) binge-eating disorder (BED), (4) avoidant/restrictive food intake disorder (ARFID), (5) pica, (6) rumination disorder, (7) other specified feeding or eating disorder, and (8) unspecified feeding or eating disorder. This chapter focuses on feeding and eating disorders most commonly seen in AYAs: AN, BN, BED, and ARFID. These feeding and eating disorders are characterized by weight-control behaviors and eating attitudes and behaviors that commonly result in medical complications. Individuals with feeding and eating disorders benefit from prompt diagnosis and aggressive multidisciplinary, developmentally appropriate treatment.

The epidemiologic and treatment data included in this chapter predate the changes in the DSM-5 and these changes are likely to affect the results of future epidemiologic and treatment studies.

ANOREXIA NERVOSA

The core features of AN include significantly low weight, fear of gaining weight, and a disturbance in the way body weight, shape, or size is experienced. There are two separate subtypes, the restricting type, AN-R (those who control their weight through dieting, fasting, or exercising) and a binge-eating/purging subtype, AN-B/P (those who purge calories to control weight and/or routinely binge-eat) (Table 33.1).¹

Etiology

The etiology of AN is multifactorial with biological, psychological, and sociocultural factors all contributing to the development of the disorder. Over the last decade, research has focused on the contributions of genetics to biological vulnerability, the personality type associated with AN, and the potential role of neurotransmitters in the etiology of the disorder.

TABLE 33.1 DSM-5 Diagnostic Criteria for Anorexia Nervosa¹

A	Restriction of energy intake relative to requirements, leading to a significantly low body weight in the context of age, sex, development trajectory, and physical health. Significantly low weight is defined as a weight that is less than minimally normal or, for children and adolescents, less than that minimally expected
B	Intense fear of gaining weight or of becoming fat, or persistent behavior that interferes with weight gain, even though at a significantly low weight
C	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 persistent lack of recognition of the seriousness of the current low body weight
Restricting type	During the last three months, the individual has not engaged in recurrent episodes of binge-eating or purging behavior (i.e., self-induced vomiting or the misuse laxatives, diuretics, or enemas). This subtype describes presentations in which weight loss is accomplished primarily through dieting, fasting, and/or excessive exercise
Binge-eating/purging type	During the last three months, the individual has engaged in recurrent episodes of binge-eating or purging behavior (i.e., self-induced vomiting or the misuse of laxatives, diuretics, or enemas)

There is a familial predisposition to eating disorders, with female relatives most often affected. There is a higher rate of AN among identical twins compared to fraternal twins. In addition, relatives of individuals with an eating disorder are at higher risk of developing an eating disorder. These findings suggest that genetic factors may predispose some people to eating disorders. To date, no single gene or combination of genes has been identified. Studies suggest that certain areas of the human genome may harbor susceptibility genes for AN on chromosome 1.²

Researchers have discovered disturbances in a number of different neurotransmitters including serotonin, norepinephrine, and dopamine in those with AN. There is evidence that starvation, binging, and excessive exercising can lead to changes in neurotransmitters, and conversely, there is evidence that neurotransmitter abnormalities can lead to these behaviors. The role of disturbances
in transmission of serotonin, a neurotransmitter known to play a role in modulating appetite, obsessional behavior, and impulsivity, has received particular interest.

Weight concerns and societal emphasis on thinness are pervasive in westernized societies, and adolescent girls tend to be more vulnerable to these influences. The slim body ideal is thought to be the key contributor to the gender differences seen in both AN and BN. In a biologically predisposed individual, feelings of ineffectiveness and loss of control during adolescence, compounded by societal pressures to be thin, can lead to dieting to obtain a sense of control. Dieting itself leads to further preoccupation with shape and weight, perpetuating the cycle. Many of the behaviors, physical signs, and symptoms seen in AN can be attributed to malnutrition.

Epidemiology

Prevalence and incidence:
- Estimated prevalence in young women is 0.3% to 0.5%.³
- Estimated incidence rate is 8 cases per 100,000 population per year.
- Incidence rates are highest in 15- to 19-year-old girls.
- Rates for partial syndrome are typically higher.
- College students: 5.2% (6.2% females and 3.4% males) have a body mass index (BMI) less than 18.5; 1.4% of undergraduates state that an eating disorder disrupted their academics; 34.7% state that they are very or slightly overweight; and 52% state they are trying to lose weight.⁴
Age:
- Commonly begins during adolescence; >90% of individuals with eating disorders are diagnosed before age 25 years.
- Peak age at onset is mid-adolescence (13 to 15 years) with a range of 10 to 25 years.
- Increasing prevalence in children and younger adolescents
Gender:
- 85% to 90% of AYAs with AN are female.
- 16.7% of adolescents under age 14 with AN are male.⁵
Comorbidity:
- May coexist with other psychiatric conditions (e.g., anxiety disorders, depression, obsessive-compulsive disorder (OCD), and substance abuse disorders)
- May coexist with medical conditions (e.g., diabetes mellitus, cystic fibrosis, and celiac disease).

Risk Factors⁶

Age and gender:
- Adolescence
- Female
Early childhood eating problems:
- Picky eating, digestive and early eating-related problems
- Struggles concerning meals
Weight concerns/negative body image/dieting:
- Adolescent girls who diet are more likely to develop an eating disorder than girls who do not diet.
Perinatal events:
- Prematurity, small for gestational age, and cephalohematoma
- Young women with a history of AN may also be at increased risk for adverse perinatal events.
Personality traits:
- Perfectionism
- Anxiety
- Low self-esteem
- Harm avoidance
- Obsessionality
Early puberty
Chronic illness:
- Increased risk in teenagers with diabetes mellitus
Physical and sexual abuse:
- Individuals who have been sexually abused have the same or only slightly higher incidence of AN as those not abused.
Family history/family psychopathology:
- Elevated rates of psychiatric disorders (anxiety disorders and mood affective disorders) in first-degree relatives of patients with AN
Competitive athletics:
- Participation in sports that place a high emphasis on body weight and appearance (e.g., ballet and gymnastics).

Clinical Manifestations

Behaviors

Dieting: May follow comments about body weight, shape, or size
Relentless pursuit of thinness:
- Initially, weight loss reinforced by positive comments from others
- Later, preoccupation with food, shape, and weight progresses and patient loses control over eating.
Distorted body image: Results in continued weight loss, leading to a state of emaciation
Unusual eating attitudes and behaviors:
- Denial of hunger
- Consumes low-calorie and/or low-fat foods
- Avoids previously enjoyed foods
- Eats the same foods at the same time each day
- Breaks food into small portions, eats foods of the same color, hides food, or secretly throws food away
- May consume large amounts of water or diet sodas with caffeine to satisfy hunger or cause diuresis
- Enjoys reading cookbooks, collecting recipes, watching cooking shows on television, cooking, and preparing food for others, although will not eat
Increased physical activity:
- May stand constantly, move arms and legs, run up and down stairs, jog, do floor exercises or calisthenics in an effort to expend energy
- As weight loss continues, activity level often increases
Purging behaviors: May include vomiting, use of diuretics, fasting, excessive exercise, or herbal remedies or complementary and alternative medicines (CAM)
Frequent weighing:
- Weighing oneself daily or multiple times a day
- Weight on the scale determines how the individual feels about him/herself
Wears baggy or layered clothing: Conceals weight loss or to keep warm
Poor self-esteem
Isolation:
- Withdrawal from friends and family
- Minimizes contact with criticizing or teasing peers
- Avoids social situations associated with food
Inflexibility: Difficulties with “set-shifting” (ability to flexibly shift a cognitive response) that may result in a strong sense of “right and wrong”
Irritability and mood changes:
- Starvation can cause mood changes
- Comorbid mental illness can contribute to mood disturbance.

Signs and Symptoms

Signs and symptoms may be minimal but can include the following:

Signs:
- Weight loss:
  - Restriction of energy intake leading to a significantly low body weight (a weight that is less than minimally normal, or for children and adolescents, less than minimally expected) in the context of age, sex growth and developmental trajectory, and physical health.
  - Any significant or unexpected weight loss or failure to make expected weight gain during a period of growth is cause for concern.
  - Physical signs of malnutrition including loss of subcutaneous tissue, temporal wasting, loss of muscle mass, and prominence of bony protuberances
- Amenorrhea:
  - Amenorrhea is no longer a criterion for the diagnosis of AN, but
  - 20% to 30% develop amenorrhea before significant weight loss; 50% develop it at the same time as the weight loss; and 25% develop it following weight loss.
  - Resumption of menses usually occurs within 3 to 6 months of achieving a weight approximately 95% of median BMI.⁷
- Pubertal delay: AN can delay the start or progression of puberty.
- Growth: There is no general agreement on the impact of AN on growth. Some studies have shown that adolescents who develop AN before growth is complete may develop growth retardation, whereas others have shown that preservation of height potential can occur because of a prolonged growth period secondary to delayed bone age. Regardless, it is important to review the growth chart to determine whether the patient has crossed growth percentiles.
- Skin and body hair:
  - Dry skin with hyperkeratotic areas
  - Yellow or orange discoloration, most noticeable on the palms and soles
  - Pitting and ridging of the nails
  - Lanugo hair—fine downy hair commonly seen on the back, stomach, or face
  - Hair loss or thinning
- Recurrent fractures
- Hypothermia: Oral body temperature may be 35°C or lower
- Bradycardia: One of the most common cardiac findings
- Hypotension: Hypotension associated with significant postural changes
- Acrocyanosis
- Edema, usually dependent
- Systolic murmur sometimes associated with mitral valve prolapse
Symptoms:
- Cold intolerance
- Postural dizziness and fainting
- Early satiety, abdominal bloating, discomfort, and pain
- Constipation
- Fatigue, muscle weakness, and cramps
- Poor concentration

Laboratory Features

Hematological:
- Leukopenia: May be a relative lymphocytosis
- Anemia: Not common, usually a late finding
- Thrombocytopenia
- Decreased serum complement C3 levels (normal C4 levels); no evidence for increased susceptibility to bacterial infection
- Decreased erythrocyte sedimentation rate (ESR); if the ESR is elevated, consider another diagnosis.
Chemistry:
- Hypokalemia: Hypokalemia with an increased serum bicarbonate level may indicate frequent vomiting or use of diuretics, whereas nonanion gap acidosis is common with laxative abuse. Caloric restriction alone does not usually cause hypokalemia.
- Hyponatremia: Secondary to excess water intake
- Hypophosphatemia
- Hypomagnesemia
- Hypocalcemia
- Increased blood urea nitrogen (BUN)
- Mildly increased serum transaminases
- Increased cholesterol
- Increased serum carotene level (15% to 40% of patients)
- Decreased vitamin A level
- Decreased serum zinc and copper levels
Endocrine:
- Thyroid:
  - Thyrotropin (TSH): Usually normal
  - Thyroxine (T₄): Usually normal or slightly low
  - 3,5,3′-Triiodothyronine (T₃): Often low, probably representing increased conversion of T₄ to reverse T₃
  - Thyroid changes represent adaptation to starvation, do not require thyroid hormone replacement, and will reverse with weight restoration.
- Growth hormone (GH):
  - Decreased insulin-like growth factor 1 levels
  - GH levels normal or elevated
- Prolactin: Usually normal
- Gonadotropins:
  - Basal levels of luteinizing hormone (LH) and follicle-stimulating hormone (FSH): Usually low
  - Twenty-four-hour LH secretory pattern: Prepubertal with low LH levels and no spikes or occasional nocturnal spikes
  - Blunted response of FSH and LH to gonadotropin-releasing hormone stimulation
- Sex steroids:
  - Estradiol: Low in females (<30 pg/mL)
  - Testosterone: Low in males
- Cortisol:
  - Basal levels normal or slightly high
  - Decreased response of adrenocorticotropic hormone (ACTH) to corticotropin-releasing hormone
  - Normal cortisol response to ACTH stimulation
Cardiac:
- Electrocardiogram (ECG): Bradycardia, low-voltage changes, prolonged QTc interval, T-wave inversions, and occasional ST-segment depression
- Echocardiogram: Decreased cardiac size and left ventricular wall thickness, pericardial effusion, and increased prevalence of mitral valve prolapse
Gastrointestinal (GI):
- Upper GI tract series: Usually normal findings; with occasional decreased gastric motility. May demonstrate features of the superior mesenteric artery syndrome
- Barium enema: Normal findings
Renal and metabolic:
- Decreased glomerular filtration rate
- Elevated BUN concentration
- Decreased maximum concentration ability (nephrogenic diabetes insipidus)
- Metabolic alkalosis
- Alkaline urine

Low bone mineral density (BMD):

Females with AN have low BMD and are at increased fracture risk.
Oral estrogen-progesterone combination pills have not been proven to be effective in increasing BMD.⁸,⁹
Bisphosphonates (alendronate and risedronate) have shown no significant effect on spine BMD in adolescents¹⁰ but positive effect in adults.¹¹

17β-estradiol transdermal patch to older girls with AN (bone age ≥ 15 years) and small but increasing doses of ethinyl estradiol to younger girls (bone age < 15 years, in whom growth is not complete) showed increased spine and hip BMD.¹² However, complete catch-up did not occur.

TABLE 33.2 Medical Complications of Eating Disorders

System	Anorexia Nervosa	Bulimia Nervosa
Fluid and electrolytes	Dehydration, elevated BUN/creatinine Hypokalemia Hyponatremia Hypochloremic alkalosis Hypophosphatemia Hypomagnesemia Hypoglycemia Ketonuria Edema	Dehydration, elevated BUN/creatinine Hypokalemia (from vomiting or from laxative or diuretic use) Hypophosphatemia (especially when binging occurs after a prolonged period of dietary restriction) Hypomagnesemia Edema
Head, eyes, ears, nose and throat	Dry, cracked lips and tongue	Dry lips and tongue Palatal scratches Erosion of dental enamel Dental caries
Cardiovascular	Bradycardia Orthostatic hypotension Orthostatic blood pressure or heart rate changes Cardiac arrhythmias Electrocardiographic abnormalities (prolonged QT interval, low voltage, T-wave abnormalities) Reduced myocardial contractility Mitral valve prolapse Pericardial effusion Congestive heart failure	Dizziness Orthostatic blood pressure or heart rate changes Cardiac arrhythmias Ipecac cardiomyopathy
Gastrointestinal	Delayed gastric emptying Constipation Elevated transaminases Superior mesenteric artery syndrome Rectal prolapse Gallstones	Parotid swelling Esophagitis Mallory-Weiss tears Rupture of the esophagus or stomach Acute pancreatitis Paralytic ileus secondary to laxative abuse Cathartic colon Barrett esophagus
Pulmonary Renal	Elevated BUN/creatinine Decreased glomerular filtration rate Renal calculi Edema Renal concentrating defect Enuresis (most commonly nocturnal)	Aspiration pneumonia Pneumomediastinum Elevated BUN/creatinine Massive edema (after withdrawal of laxatives)
Endocrine	Primary or secondary amenorrhea Pubertal delay Growth retardation and short stature Low T3 syndrome Hypercortisolism Partial diabetes insipidus	Irregular menses
Hematological	Anemia Leukopenia Thrombocytopenia Low ESR
Musculoskeletal	Muscle wasting and generalized muscle weakness Reduced BMD Increased fracture risk	Fatigue, muscle weakness, and cramps Reduced BMD (if previously at a low weight or amenorrheic)
Dermatologic	Acrocyanosis Dry, yellow skin (hypercarotenemia) Lanugo Brittle nails Thin, dry hair Hair loss	Calluses on the dorsum of hand (Russell’s sign)
Neurological	Syncope Seizures Peripheral neuropathies Structural brain changes (enlarged lateral ventricles and deficits in both gray and white matter volumes) Decreased concentration, memory, and thinking ability	Syncope Seizures

Current recommendations for low BMD in AN include sustainable weight restoration through optimizing nutritional intake, resumption of spontaneous menses, and optimal calcium (1,300 mg/day of elemental calcium) and vitamin D (600 to 1,000 IU units/day) intake. Despite intervention, BMD may not return to normal.