Perhaps no illnesses cross the spectrum of medical and behavioral health more than the eating disorders. Anorexia nervosa alone has the highest mortality rate of any mental health diagnosis and most of these deaths are due to medical complications.1 Although bulimia nervosa and binge-eating disorder are less lethal, they too commonly result in significant medical complications. Emotional symptom overlay from comorbid psychiatric illness often confounds the medical diagnostic picture. The fear and shame associated with food intake and body image may manifest in physical symptoms that make assessment and treatment more challenging. In addition, the contemporary medical issues of food allergies and gluten enteropathy, among others, continue to complicate the treatment of eating disorders requiring a careful and methodical diagnostic regimen and accuracy in evaluation given the lifelong impact they have on a person's nutrition, particularly when an eating disorder is present. Furthermore, primary care and specialty providers are often not educated extensively about eating disorders so what may seem clear to one provider treating one facet of a traditional medical illness may involve a more complex issue requiring specialty care in eating disorders to diagnose and treat these illnesses in the most efficacious and cost-effective manner. Exhaustive testing for physical symptoms is not always needed when it is clear that the patient is manifesting an eating disorder.1
Medical complications of eating disorders range from minor and annoying to severe and life-threatening. Many medical complications can be predicted by eating disorder behaviors and the relative time spent engaging in each of the behaviors (Table 1). For example, anorexia nervosa, bulimia nervosa, and binge-eating disorder may all involve food restriction, yet the metabolic changes manifested as a result are dependent on the frequency and severity of restriction as offset by bingeing or as impacted by the compensatory behaviors of purging. Simply manifesting the behavior infrequently may not produce significant medical or laboratory findings, whereas severe daily restricting, particularly with weight loss, will usually result in an adaptive metabolic response that lowers metabolism by involving the hypothalamic neuroendocrine axis.2 This adaptive change decreases metabolic demand and thus results in fewer calories being needed to sustain life.3
Eating Disorder Symptoms and Associated Potential Medical Complications
An important concept to understand is that end weight does not necessarily reflect the severity of the metabolic impact of an eating disorder. The reduction in metabolism and subsequent impact is similar in people at higher weights that drop to a normal body weight in a relatively short period as compared to a person with anorexia nervosa who drops from a low body weight to a lower weight. Likewise, associated symptoms such as irregular menses or amenorrhea may occur in someone who appears to be at a normal weight that may be low relative to her lifetime high weight.
A patient's condition takes on new seriousness and becomes particularly dangerous once vital signs are impacted. This may occur at any body weight. The reduction in metabolic rate in many cases is responsible for a significant change in vital signs with serious clinical impact. Hypothermia is common, given the extensive caloric requirement to maintain a normal body temperature.1 As the hypothermia and metabolic change progresses, the patient becomes increasingly symptomatic, withdrawn, and isolating. They may appear depressed, yet if related to physiologic changes, the cognitive changes improve dramatically with refeeding in a relatively short period.1 Bradycardia (heart rate <60 bpm) and hypotension (systolic blood pressure <90 mm Hg or diastolic blood pressure <50 mm Hg) are frequently found in patients with anorexia nervosa.3 In fact, a relative tachycardia (70–100 bpm) in a patient with moderate to severe anorexia nervosa may be an ominous sign of impending cardiac failure.4 Admission with telemetry monitoring should be considered for adults with a heart rate <40 bpm and children and adolescents with a heart rate near 40 bpm.5 A history of compulsive exercise with increased vagal tone may exacerbate the bradycardia of metabolic reduction.
Restricting may cause significant medical complications primarily involving changes in the hypothalamic neuroendocrine axis. The actual metabolic change results from a shift in iodination of the most metabolically active thyroid hormone T3 (triiodothyronine) to reverse T3, which is less metabolically active.3 There is a concomitant reduction in noradrenergic activity in the central and peripheral nervous system, which may lead to hypothermia, bradycardia, and hypotension. The autonomic instability resulting from these changes causes orthostasis with significant changes in supine and standing blood pressure and pulse.4 The extent to which they are impaired is indicative of the severity of the restricting impact on the individual. Orthostatic vital signs are recorded regularly during treatment to monitor the response to refeeding but may take some time to normalize. Some people may be diagnosed by professionals who do not specialize in eating disoders as having manifesting postural orthostatic tachycardia syndrome, which is often inaccurate. An inaccurate diagnosis is particularly problematic if the patient is started on oral steroids to counter the metabolic impact. The steroids may have an adverse effect on bone health, which is problematic for many people with eating disorders.
Fluid Restricting and Fluid Loading
Some people with eating disorders may inadvertently or intentionally dehydrate themselves by excessively restricting fluids. They may indicate that they prefer that “washed out” feeling of dehydration and some have even reported that their skin “feels less tight.” Some may water load, drinking copious amounts of water attempting to maintain satiety with zero calories, whereas others fear their weigh-in appointments and drink excessive fluids trying to influence their weight and avoid further meal plan calorie increases. Fluid restricting can lead to serious dehydration, which then causes changes in the angiotensin-renin system with an increase in serum aldosterone thus affecting fluid retention. If fluid intake is suddenly normalized without compensatory purging, which occurs in intensive eating disorder treatment, a pseudo-Bartter syndrome can develop, resulting in significant fluid retention and edema.1
Voluntary vomiting, depending on frequency and timing with meal consumption, can result in weight loss and dehydration. People who vomit may induce it with their finger, toothbrush, or spoon. Eventually many learn to vomit spontaneously with little effort. The lower esophageal sphincter may become lax and contribute to the development of significant gastroesophageal reflux disease. This is associated with a risk of chronic inflammation of the esophagus with resultant metaplastic changes to the epithelial lining causing Barrett's esophagus, a premalignant condition requiring careful surveillance and treatment.3 Recurrent vomiting may also cause hypertrophy of the salivary glands, dental caries, and loss of dental enamel. Infrequently, chronic vomiting can cause a Mallory-Weiss tear of the stomach with potential for significant loss of blood. A full or microperforation of the esophagus3 is also possible with a risk of mediastinitis and sepsis. Loss of fluids with excessive vomiting can lead to dehydration, which can exacerbate the hypotension and orthostasis seen with metabolic changes and autonomic insufficiency. Electrolyte imbalances, particularly hypokalemia, can cause potentially lethal arrhythmias.6
Laxatives may be used in an attempt to “push” the food through the colon to avoid absorption, although it is ineffective for that use. Laxative misuse has the potential to permanently alter normal bowel function and cause dehydration and electrolyte imbalances. Dosing of over-the-counter stimulant laxatives often escalates due to tolerance.
Diuretic abuse is typically due to a sensation of “bloating” or a belief that one is “swollen” from fluid. This is often related directly to body image issues and can cause dehydration and electrolyte imbalances.
Diet pill abuse can cause diastolic hypertension, palpitations, and tremor. The potential for arrhythmias including those that are potentially lethal is always a risk. Ephedra products have been particularly worrisome as a potential cause for lethal arrhythmias and are banned by the US Food and Drug Administration, although they are available on the Internet internationally.4
Ipecac has long been used to induce vomiting; however, it is highly myotoxic and particularly cardiotoxic with a risk of cardiomyopathy with continued use. Ipecac has been taken off store shelves and its use appears to have become less frequent.4
Binge eating is seen in some cases of anorexia nervosa, bulimia nervosa, and binge-eating disorder. Restricting post-binge episode is not uncommon, and it is the relative time in bingeing versus restricting that determines weight. Typically, the more frequent the binge episodes, the higher the body weight. The impact of binge-eating disorder with weight gain is usually consistent with the physical impact of obesity including hypertension, hyperlipidemia, metabolic syndrome or type 2 diabetes, and joint deterioration.7
Physical Impact of Eating Disorders by Organ Systems
Eating disorders affect almost every organ in the body. Involution of some organs from malnutrition conserves calories. Some organs such as the heart, uterus, ovaries, and testicles return to normal size with normalization of nutrition and return to a healthier body weight.6 Of particular interest is the brain, which manifests volume loss with prolonged starvation.8 It is unclear as to whether or not full brain volume restoration is possible with long-term nutritional and weight restoration.
The skin shows numerous changes, particularly with anorexia nervosa. Lanugo hair on the extremities is a classic finding in anorexia nervosa. With metabolic changes of malnutrition at any weight, hair loss can be problematic with hair follicles prematurely entering a dormant phase. This is one finding that can cause great alarm for patients and may encourage them to seek medical attention. Both conditions resolve with attainment of normal nutrition and weight.3
Cardiovascular impact is of great concern and cardiac failure, electrolyte imbalances, and subsequent fatal arrhythmias are key factors in many deaths from eating disorders.1 Of particular concern is the development of a prolonged QT interval. This can lead to torsades de pointes and subsequent ventricular fibrillation and death.1 Often severe hypokalemia or hypomagnesemia are implicated from vomiting, laxative, or diuretic abuse. More recently QT dispersion or the interlead variation in the QT-segment length has taken on new interest as a predictor for arrhythmias.9 Patients with anorexia nervosa may have a 2-fold or greater increase in QT dispersion that correlates with the severity of their weight loss and reduced metabolic rate.9 The QTc and QT dispersion both normalize with refeeding.
Anatomic changes in the heart have also been noted with prolonged starvation.1,4 There is lowered physiologic demand due to metabolic reduction to conserve on caloric expenditure. The left ventricle is particularly impacted, and a loss of up to 25% of the volume of the left ventricle has been noted in anorexia nervosa.4 The heart valves may be affected with the structural changes of the heart. This can lead to valvular incompetence and mitral valve prolapse. This may manifest with chest pain or palpitations and be quite concerning. Cardiac changes in general, including anatomic changes, normalize with full weight restoration and proper nutrition.4
The impact of the eating disorder on the oral cavity includes dental caries and glandular hypertrophy from vomiting.4 Chronic vomiting can also cause esophagitis and gastritis. Occasionally hematemesis occurs with vomiting which may result from a small superficial laceration of the mouth or throat or may occur from inflammation of the gastrointestinal tract or even a Mallory-Weiss tear with subsequent hemorrhage. Gastroparesis from metabolic changes are problematic and present as abdominal pain and bloating upon refeeding. Constipation and hemorrhoids from constant straining of the stool are extremely common. Symptomatic treatment is routinely used acutely, however, the symptoms typically slowly resolve with full weight and metabolic restoration. Chronic laxative use may cause a cathartic colon from nerve plexus damage necessitating continued nonstimulant laxative use or a subtotal colectomy in rare cases.10
Secondary amenorrhea in adults or primary amenorrhea in adolescents is found in anorexia nervosa and to some extent in bulimia nervosa, although irregular menses is more common.3 In some patients, the menstrual irregularity may precede the onset of weight loss. These symptoms are related to an energy imbalance resulting in a “hypothalamic amenorrhea syndrome” with variable reduction in pulsatile hypothalamic gonadotropin-releasing hormone signaling the pituitary gland, resulting in a failure of ovulation.4 Although some patients come to eating disorder treatment having been started on hormone therapy (eg, estrogen plus progestin) to induce menses, there is little evidence to show any benefit.4 In the short-term, it may be more beneficial to observe the resumption of normal menses with weight restoration. In general, resumption of menses requires attaining 90% to 100% of ideal body weight, and it may take as many as 1 to 6 months after reaching and maintaining a healthy weight before regular menstruation resumes.3 Although reproductive function is severely impacted by anorexia nervosa, outcome studies suggest that with full recovery, fertility may not be impaired.4
With severe malnutrition and weight loss there is significant loss of muscle mass and function, yet muscle is very responsive to refeeding. Dyspnea is not uncommon and often related to the direct physiologic impact on the muscles of respiration, yet they are often the first to recover with refeeding and the dyspnea resolves.
Bone health can be severely impacted by malnutrition, low body weight, and amenorrhea and is not readily reversible. Osteopenia is common in anorexia nervosa occurring in up to 92% of women with the disorder, whereas osteoporosis is present in almost 40%.11,12 Significant demineralization of bone has been found in adolescents with even a brief course of anorexia nervosa.11 Osteoporosis is estimated to occur in more than one-half of adolescent and young adult females with eating disorders. Patients with anorexia nervosa have a fracture rate 7 times higher than women without eating disorders.4 Full weight restoration and nutritional restoration along with resumption of menses is key to preventing further bone loss. Supplemental vitamin D and calcium should be given, and weight-bearing exercise should be avoided unless it is carefully monitored during the weight restoration process. If there is a likelihood of bone loss continuing or fracture risk is particularly high, physiologic transdermal estrogen plus oral progesterone, bisphosphonates (alendronate or risedronate), or teriparatide could be considered.11 Other agents, such as denosumab and testosterone in men, have not been tested in populations of people with eating disorders.
Eating Disorders and Gluten Enteropathy and Food Allergies
People with eating disorders claiming to have gluten enteropathy and food allergies have become increasingly common given the widespread reporting of these illnesses in contemporary medical news reports.13 Although the rate of patients with eating disorders with gluten enteropathy is unknown, the incidence of true non-Celiac gluten sensitivity is estimated at 1% to 13% of the population in the United States.14 Given the lifelong nature of gluten sensitivity and food allergies, patients coming to eating disorder treatment should have a thorough evaluation to root out potential gluten sensitivity and food allergies to verify the existence of these long-term illnesses affecting nutritional intake.
Eating Disorders and Diabetes Mellitus
Insulin withholding for weight loss in people with type 1 diabetes, known as eating disorder diabetes mellitus type 1 (EDDMT1),15 has been reported more in recent years. The physical impact of EDDMT1 in people with type 1 diabetes and anorexia nervosa is severe, and the crude mortality rate is up to 35%.4 The risk of diabetic ketoacidosis is substantial and indeed life-threatening. The risk of retinopathy and nephropathy is markedly increased with this dual-diagnosis illness.
Patients with infrequent symptoms and minimal weight loss may show no laboratory evidence of impairment from an eating disorder. Likewise, patients with weight loss that occurs slowly over a longer period of time may also show no abnormalities. Otherwise, common findings include leukopenia, anemia, hypokalemia, hypomagnesemia, hypophosphatemia, and liver function elevations with hepatic injury from malnutrition. Refeeding itself can cause liver function elevations with refeeding hepatitis and hypophosphatemia. Decreased hepatic glycogen stores in the liver may cause hypoglycemia (blood sugar <60 mg/dL), which can be particularly dangerous and requires careful monitoring. Thyroid function abnormalities consistent with euthyroid sick syndrome include normal to mildly elevated thyroid-stimulating hormone levels with slightly decreased T3 and T4 levels. As mentioned previously, hyponatremia is common in people who water load.
The multisystem impact of eating disorders on medical stability and long-term medical morbidity necessitate comprehensive medical care simultaneously coordinated with the mental health component of treatment. At times the separation of emotionally based physical complaints and those with a true underlying medical etiology is blurred. A comprehensive medical evaluation is of prime importance in management of the eating disorder with careful consideration of medical concerns that heighten the risk of premature death or serious medical morbidity.
- Mehler P, Andersen A, ed. Eating Disorders, A Guide to Medical Care and Complications. 3rd ed. Baltimore, MD: The Johns Hopkins University Press; 2017.
- Steinglass JE, Walsh BT. Neurobiological model of the persistence of anorexia nervosa [published online ahead of print May 18, 2016]. J Eat Disord. doi:10.1186/s40337-016-0106-2 [CrossRef].
- Mehler PS, Birmingham CL, Crow SJ, Jahraus JP. Medical complications of eating disorders. In: Grilo CM, Mitchell JE, eds. The Treatment of Eating Disorders–A Clinical Handbook. 1st ed. New York, NY: Guilford Press; 2011:66–80
- Devlin M, Jahraus J, DiMarco I. Eating disorders. In: Levenson J, ed. Psychosomatic Medicine. 2nd ed. Washington, DC: American Psychiatric Association; 2010:305–333.
- Yager J, Devlin MJ, Halmi KA, et al. Practive guideline for the treatment of patients with eating disorders. 3rd ed. https://psychiatryonline.org/pb/assets/raw/sitewide/practice_guidelines/guidelines/eatingdisorders.pdf.
- Academy for Eating Disorders. Eating Disorders, A Guide to Medical Care, Critical Points for Early Recognition & Medical Risk Management in the Care of Individuals with Eating Disorders. 3rd ed. Reston, VA: Academy for Eating Disorders; 2016.
- Thornton LM, Watson HJ, Jangmo A, et al. Binge-eating disorder in the Swedish national registers: somatic comorbidity. Int J Eat Disord. 2017;50(1):58–65. doi:. doi:10.1002/eat.22624 [CrossRef]
- Roberto CA, Mayer LE, Brickman AM, et al. Brain tissue volume changes following weight gain in adults with anorexia nervosa. Int J Eat Disord. 2011;44(5):406–411. doi:. doi:10.1002/eat.20840 [CrossRef]
- Sachs KV, Harnke B, Mehler PS, Krantz MJ. Cardiovascular complications of anorexia nervosa: a systematic review. Int J Eat Disord. 2016;49(3):238–248. doi:. doi:10.1002/eat.22481 [CrossRef]
- Mascolo M, Geer B, Feuerstein J, Mehler PS. Gastrointestinal comorbidities which complicate the treatment of anorexia nervosa. Eat Disord. 2017;25(2):122–133. doi:. doi:10.1080/10640266.2016.1255108 [CrossRef]
- Misra M, Golden NH, Katzman DK. State of the art systematic review of bone disease in anorexia nervosa. Int J Eat Disord. 2016;49(3):276–292. doi:. doi:10.1002/eat.22451 [CrossRef]
- Drabkin A, Rothman MS, Wassenaar E, Mascolo M, Mehler PS. Assessment and clinical management of bone disease in adults with eating disorders: a review. J Eat Disord. 2017;5:42. doi:. doi:10.1186/s40337-017-0172-0 [CrossRef]
- NIAID-Sponsored Expert Panel Guidelines for the diagnosis and management of food allergy in the United States: report of the NIAID-sponsored expert panel. J Allergy Clin Immunol. 2010;126:S1–S58. doi:. doi:10.1016/j.jaci.2010.10.007 [CrossRef]
- Riddle MS, Murray JA, Porter CK. The incidence and risk of celiac disease in a healthy US adult population. Am J Gastroenterol. 2012;107(8):1248–1255. doi:. doi:10.1038/ajg.2012.130 [CrossRef]
- Criego A, Jahraus J. Eating disorders and diabetes. Diabetes Spectr. 2009;22(3):135–162. doi:. doi:10.2337/diaspect.22.3.135 [CrossRef]
Eating Disorder Symptoms and Associated Potential Medical Complications
||Altered metabolism with hypothermia, cognitive impairment, dizziness, hypotension, bradycardia, orthostasis, amenorrhea, edema, fatigue
||Obesity, hypertension, hyperlipidemia, insulin resistance, joint deterioration, dyspnea, sleep apnea, gallbladder disease
||Electrolyte imbalance (hypokalemia), arrhythmias, esophagitis/gastritis, gastroesophageal reflux disease, dental caries, dehydration, alkalosis, parotid/submandibular gland hypertrophy
||Cathartic colon, dehydration, electrolyte imbalance, metabolic acidosis, alkalosis
||Dehydration, electrolyte imbalance
|Appetite suppressant abuse
||Hypertension, tremor, arrhythmias
||Hyponatremia, headache, nausea, dizziness, seizure
||Severe bradycardia, joint deterioration, stress fractures, overuse syndromes