Food restriction related to eating disorders like, anorexia nervosa and ARFID, can lead to malnutrition. Malnutrition can cause serious, whole-body complications impacting every organ in the body–from brain fog and brittle bones to cardiac issues and hormone changes. This guide can help you better understand the health risks related to malnutrition, supporting recovery.

Malnutrition, Food Restriction, & Eating Disorders

Food restriction in some form is an essential criterion present in several eating disorder classifications. This restriction can take the form of:

• No food intake
• Eating minimal amounts of food
• Only eating specific foods
• Eating specific amounts of food
• Fasting for large portions of the day

Prolonged food restriction often leads to malnutrition, impacting every organ system and causing a variety of medical complications.

Food Restriction & Eating Disorder Diagnoses

Several eating disorders feature restriction within the diagnostic criteria, including the restrictive subtype of anorexia nervosa (AN-R), avoidant restrictive food intake disorder (ARFID) and other specified feeding or eating disorder (OSFED).

Anorexia Nervosa

Food restriction is most often associated with anorexia nervosa (AN). AN is an eating disorder categorized by:

• Restriction of energy intake relative to requirements, leading to significantly low body weight in the context of age, sex, developmental trajectory, and physical health
• Intense fear of gaining weight or becoming fat or persistent behavior that interferes with weight gain
• Disturbed by one’s body weight or shape, self-worth influenced by body weight or shape, or persistent lack of recognition of the seriousness of low body weight

Avoidant/Restrictive Food Intake Disorder (ARFID)

People with ARFID might avoid food-related sensory experiences, have a fear of adverse consequences or display a lack of interest in food. ARFID is also categorized by:

• Significant weight loss (or failure to achieve expected weight gain or faltering growth in children)
• Significant nutritional deficiency
• Dependence on enteral feeding or oral nutritional supplements
• Marked interference with psychosocial functioning

Unlike other eating disorders, ARFID features no image concerns, fear of gaining weight, or desire for thinness. While individuals with ARFID do not purposefully restrict their food intake with the intent to limit their energy intake or initiate weight loss like anorexia nervosa or bulimia nervosa (BN), their eating disturbance can still cause malnutrition.

Other Specified Feeding or Eating Disorder (OSFED)

According to the DSM-5, the category of other specified feeding or eating disorder (OSFED) applies to individuals experiencing significant distress due to symptoms similar to eating disorders but who do not meet the full criteria for diagnosing one of these disorders. “Atypical” anorexia (below) is an eating disorder that falls under OSFED.

“Atypical” Anorexia Nervosa
“Atypical” anorexia nervosa (A-AN) is characterized by an individual either meeting all the criteria for anorexia nervosa except their final weight is at or above their ideal body weight (IBW). A-AN may also be diagnosed when some but not all of the criteria for AN are met. For example, the symptoms have occurred for less than three months.

Complications from Restriction & Malnutrition

The medical complications of eating disorders affect the entire body, from head to toe. Patients who have been restricting food are often malnourished, leading to neurological, musculoskeletal, gastrointestinal, cardiovascular, pulmonary, hepatic, endocrine, and dermatological problems.

Neurological Complications

Brain Fog
Prolonged starvation affects the entire body, including the brain. Patients typically report “brain fog,” a catch all term that refers to a decline in concentration, memory, and cognitive flexibility and function.

Brain Atrophy
Brain atrophy, or a “starved brain,” is a loss of brain mass due to severe malnutrition. Brain atrophy can be significant in patients with eating disorders, particularly those with AN. Magnetic resonance imaging (MRI) will often show significant loss of brain mass. Brain atrophy impacts both white and grey matter in the brain. This may contribute to various cognitive, emotional, and motivational processing deficits.

Musculoskeletal Complications

Decreased Bone Mineral Density
As individuals with eating disorders lose weight, their body composition changes. They begin losing lean muscle mass. They may also lose essential bone growth since the forces exerted on bones via muscle contraction are what cause increased bone growth.

A lower weight, combined with diminished activity and decreased skeletal muscle mass due to malnutrition, decreases bone mineral density over time. This puts individuals with eating disorders at risk for developing osteopenia, osteoporosis, and fractures. Hormonal changes also contribute to reduced bone mineral density. Decreased bone mineral density is more common in individuals with a lower age of onset, as bone accrual peaks during adolescence.

Osteopenia & Osteoporosis
Osteopenia (mild loss of bone mineral density) and osteoporosis (severe loss of bone mineral density) are some of the most common medical complications of eating disorders. About 40% of women with AN have osteoporosis and about 92% have osteopenia.

Brittle Bones
Decreased bone mineral density and poor bone health increase an individual’s risk for lifetime fractures. AN is associated with a three-fold increase in lifetime risk of fracture. Around 57% of women with AN sustain at least one fracture in their lifetime.

Those with a younger age of eating disorder onset may never reach peak bone mass. This puts them at risk for other problems with their bones and joints, including:

• Chronic pain from bone fractures
• Reduced strength and mobility
• Shorter stature

Gastrointestinal Complications

Gastroparesis
Food restriction, accompanied by a weight loss of 15-20% under the ideal body weight, is almost universally followed by gastroparesis, or delayed gastric emptying. Gastroparesis symptoms of bloating, fullness and nausea can worsen as patients eat fiber-rich foods to promote gastrointestinal transit, due to the longer digestion times.

Slow Transit Constipation
Gastroparesis, constipation, and bloating frequently accompany weight loss and malnutrition. Many patients with eating disorders report an infrequent or small stool. Like the slowed emptying of the stomach, intestinal transit time is also prolonged. This is likely a compensatory mechanism to increase nutrient uptake.

People with eating disorders may begin increasing their fiber intake or using bulking laxatives in an attempt to produce a bowel movement. This will often lead to worsening symptoms due to the effects on gastroparesis.

Superior Mesenteric Artery Syndrome
Significant weight loss causes atrophy of the mesenteric fat pad surrounding the superior mesenteric artery (SMA), causing the angle between the SMA and the aorta to narrow, thereby compressing the duodenum. This is associated with abdominal pain after eating, early satiety, nausea, and vomiting.

Dysphagia (difficulty swallowing)
Patients can experience functional or oropharyngeal dysphagia. The muscle loss and weakness associated with severe food restriction and excessive weight loss can impact the throat muscles responsible for swallowing. This can lead to oropharyngeal dysphagia, where it becomes difficult to move food, liquid, or saliva from the mouth to the throat. A small study suggests that oropharyngeal dysphagia occurs most often in critically ill patients with anorexia nervosa.

Cardiovascular Complications

Bradycardia
Bradycardia, a heart rate under 60 beats per minute, is the most common medical complication in eating disorder patients. Bradycardia occurs in up to 95% of patients with AN. It frequently presents as the first medical implication of an eating disorder.

It is suggested that heightened vagal tone is the cause of bradycardia, as the body attempts to conserve energy. However, findings to support this have been inconsistent. Bradycardia can also contribute to syncope (fainting) and cardiac pauses, with the latter potentially leading to more catastrophic arrhythmias.

Hypotension
Hypotension is another common cardiovascular issue in eating disorder patients. Chronic malnutrition causes the body to break down tissue for fuel, including muscle tissue. It is indiscriminate in the tissues it affects and includes the heart, causing decreased cardiac muscle as well. This can be associated with the following symptoms:

• Dizziness
• Nausea
• Fatigue
• Blurred vision
• Cold, clammy skin
• Confusion
• Tachycardia (fast heart rate)

Pericardial Effusion
Fluid around the heart (pericardial effusion) is presumed to develop in about 25% of those with AN. It may be related to fat and cardiac atrophy or potentially abnormal thyroid hormone but is only rarely a cause of concern. In rare instances when excess fluid builds up surrounding the heart, a condition called cardiac tamponade can develop, leading to reduced cardiac output.

Pulmonary Complications

Aspiration Pneumonia
Dysphagia can cause aspiration pneumonia when food or liquid is breathed into the airways or lungs instead of being swallowed into the esophagus. This can lead to inflammation and/or infection.

Emphysema
Some studies suggest emphysema can develop in patients with eating disorders, regardless of smoking history. In emphysema, the lungs’ alveoli (air sacs) are damaged. This causes them to rupture and create a larger space instead of the typical, smaller spaces. This reduces the surface area available for gas exchange, causing:

• Shortness of breath
• Coughing
• Fatigue

Pneumothorax
Being malnourished increases the risk for collapse of the lung, or pneumothorax. Both those who restrict and those who purge seem to be at risk for this condition. Pneumothorax typically presents with shortness of breath and chest pain.

Hepatic Complications

Abnormal Liver Transaminases (AST & ALT)
Liver transaminases (AST & ALT) are often abnormal in people with AN. Greater severity of weight loss contributes to increased elevation in the AST and ALT. It is more likely to occur in patients with a body mass index (BMI) less than 12/kg/m2. It is seemingly caused by autophagy, or programmed cell death. Refeeding can be another cause of increased AST and ALT, known as refeeding hepatitis.

Endocrine dysfunction

Euthyroid Sick Syndrome
The malnutrition associated with food restriction can cause the hypothalamic-pituitary-thyroid axis to become dysregulated. Euthyroid sick syndrome, or nonthyroidal illness syndrome, is most commonly characterized by low triiodothyronine (T3) and thyroxine (T4) levels with low to normal thyroid stimulating hormone (TSH). To conserve energy, the malnourished body converts T4 to the inactive reverse T3 in the periphery instead of the active T3 hormone.

Abnormal Glucose Metabolism & Hypoglycemia
Prolonged starvation can cause low levels of blood glucose (hypoglycemia). Coupled with a low BMI, insulin levels are also low. Insulin helps the body utilize blood sugars for metabolism. Reduced insulin levels contribute to the body using fats/proteins as an energy substrate, creating a state of catabolism. The body remains at high risk for hypoglycemia, which can result in coma and death due to depleted glycogen stores.

Cortisol Dysregulation
Cortisol, the body’s primary stress hormone, is up regulated in starvation. There also appears to be increased levels of corticotropin-releasing hormone (CRH), a hormone secreted from the hypothalamus that increases the production of cortisol. Cortisol plays a vital role in regulating metabolism, but it can also impact the immune response. This can increase bone breakdown and contribute to the development of gastritis.

Low Sex Hormones
Malnutrition can cause low sex hormones in both men and women. Disruption of the hypothalamic-pituitary-gonadal axis causes hypothalamic hypogonadism. This can cause decreased estrogen, amenorrhea, and infertility in women. It can also cause low testosterone levels, lowered sex drive, and reduced sexual function in men.

Typically, the hypothalamus secretes gonadotropin-releasing hormone (GnRH) in a pulsatile manner, causing increased secretion of luteinizing hormone (LH) and follicle-stimulating hormone (FSH) from the pituitary gland. This causes the production of various hormones from the ovaries or testes, ultimately resulting in increased levels of progesterone and estradiol in females and testosterone in males.

Dermatological Signs

Dry and Itchy Skin
Dry skin (xerosis) is seen in almost all patients with severe malnutrition. Dry skin can range from mild dryness to scalier skin. Prolonged starvation reduces the activity of the sebaceous glands, which produce sebum (lubricating oil) for the skin and hair, causing dry skin. Patients with eating disorders frequently have itchy skin (pruritis), with xerosis contributing to this.

Lanugo-like Body Hair
Lanugo-like body hair is fine, downy, and pigmented hair on various body parts. Lanugo-like body hair is frequently seen in eating disorder patients, particularly younger patients, and typically doesn’t appear in other forms of chronic malnutrition. It may also be an attempt of the body to conserve heat.

Hair Loss
Hair loss (telogen effluvium) is another common feature of eating disorders. The hair loss typically follows a diffuse pattern, occasionally with frontal prominence. There is usually an increased number of telogen hairs and opaque hairs.

Carotenoderma
Individuals with an eating disorder may opt to eat carotenoid-rich vegetables because they are low in calories. Carotenoids are classes of yellow, orange, and red fat-soluble pigments. They give plants their color, including foods like tomatoes, pumpkins, and carrots. When excessively consumed, they deposit orange or yellow pigment into the skin, causing orange-yellow discoloration, called carotenoderma. It can also affect the nails.

Acrocyanosis
Acrocyanosis is when the extremities develop a bluish appearance. It is suggested that acrocyanosis is an extreme form of heat conservation.

Raynaud’s Phenomenon
Acrocyanosis occurs during Raynaud’s phenomenon, which can also be characteristic of malnutrition. Acrocyanosis means bluish discoloration of the extremities due to decreased oxygen delivered to the peripheral part. It is a persistent disorder without episodic triphasic color response. Acrocyanosis is usually painless and is often triggered by heat, cold, or stress. [15]

Cheilitis & Angular Stomatitis
Riboflavin and vitamin deficiencies in eating disorder patients may cause angular stomatitis, an inflammatory skin condition of the corners of the mouth that causes painful, cracked sores. Patients can also experience cheilitis (inflammation of the lips).

Nail Dystrophy
Other than yellowing nails caused by carotenoderma and fragile nails due to xerosis, prolonged starvation can cause other problems with the nails. Iron deficiency can cause koilonychia, spoon nails, and nails with significant dips. Patients with eating disorders also report periungual edema (swelling around the nail), which may contribute to onychocryptosis (ingrown toenails).

Slow Wound Healing
Patients with eating disorders may experience slower wound healing. Zinc deficiency may further contribute to poor wound healing.

Vitamin & Mineral Deficient Diseases

Malnutrition can also cause vitamin and mineral deficiencies that cause several diseases:

• Pellagra (vitamin B3 deficiency)
• Scurvy (vitamin C deficiency)
• Acrodermatitis enteropathica (zinc deficiency-BB1)

Recognizing the serious health effects of malnutrition related to eating disorders is critical for timely intervention and recovery.

Dennis Gibson, MD, FACP, CEDS serves as the Clinical Operations Director at ACUTE. Dr. Gibson joined ACUTE in 2017 and has since dedicated his clinical efforts to the life-saving medical care of patients with extreme forms of eating disorders and severe malnutrition. Dr. Gibson is also an Associate Professor of Medicine at the University of Colorado School of Medicine. He completed his undergraduate degree at Albion College in Michigan and earned his medical degree at Southern Illinois University. He completed his internal medicine residency at University of South Florida, is Board certified in Internal Medicine and earned the prestigious CEDS credential from iaedp, underscoring his commitment to effective care and clinical excellence in the treatment of eating disorders. For more information about ACUTE Center for Eating Disorders & Severe Malnutrition, please visit acute.org.

References

• American Psychiatric Association. (2013). Feeding and Eating Disorders. In Diagnostic and statistical manual of mental disorders (5th ed.). https://doi.org/10.1176/appi.books.9780890425596.
• Grinspoon, S., Thomas, E.R., Pitts, S., et al. (2000). Prevalence and predictive factors for regional osteopenia in women with anorexia nervosa. Annals of Internal Medicine
• Holmes, S. C., Sabel, A. L., Gaudiani, J. L., Gudridge, T. A., Brinton, J. T., & Mehler, P. S. (2016). Prevalence and management of oropharyngeal dysphagia in patients with severe anorexia nervosa: A large retrospective review.
• International Journal of Eating Disorders, 49(2), 159–166. https://pubmed.ncbi.nlm.nih.gov/26316316/
• Kano, M., Muratsubaki, T., Von Oudenhove, L., et al. (2017). Altered brain and gut responses to corticotropoin-releasing hormone (CRH) in patients with irritable bowel syndrome. Scientific Reports, 7, 12425. https://www.nature.com/articles/s41598-017-09635-x
• Mehler, P. S., & Andersen, A. E. (2022). Eating Disorders: A Comprehensive Guide to Medical Care and Complications (fourth edition). Johns Hopkins University Press.
• Mehler, P. S., & Brown, C. (2015). Anorexia nervosa – medical complications. Journal of Eating Disorders, 3(1). https://doi.org/10.1186/s40337-015-0040-8
• Mehler, P. S., Krantz, M. J., & Sachs, K. (2015). Treatments of medical complications of anorexia nervosa and bulimia nervosa. Journal of Eating Disorders, 3(1). https://doi.org/10.1186/s40337-015-0041-7
• Nitsch, A., Kearns, M., Mehler, P. (2023). Pulmonary complications of eating disorders: A literature review. Journal of Eating Disorders, 11(1), 12.
• Rosen, E., Bakshi, N., Watters, A., et al. (2017). Hepatic complications of anorexia nervosa. Digestive Diseases and Sciences, 62(11), 2977-81.
• Steinman, J., & Shibli-Rahhal, A. (2019). Anorexia Nervosa and Osteoporosis: Pathophysiology and Treatment. Journal of Bone Metabolism, 26(3), 133. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6746661/
• Strumia, R. (2005). Dermatologic Signs in Patients with Eating Disorders. American Journal of Clinical Dermatology, 6(3), 165–173. https://doi.org/10.2165/00128071-200506030-00003
• Usdan, L. S., Khaodhiar, L., & Apovian, C. M. (2008). The Endocrinopathies of Anorexia Nervosa. Endocrine Practice, 14(8), 1055–1063. https://doi.org/10.4158/ep.14.8.1055
• Wang, X., Luscombe, G., Boyd, C., Kellow, J., & Abraham, S. (2014). Functional gastrointestinal disorders in eating disorder patients: Altered distribution and predictors using ROME III compared to ROME II criteria. World Journal of Gastroenterology, 20(43), 16293. https://doi.org/10.3748/wjg.v20.i43.16293
• Wong, H. K., Hoermann, R., & Grossmann, M. (2019). Reversible male hypogonadotropic hypogonadism due to energy deficit. Clinical Endocrinology. https://doi.org/10.1111/cen.13973
• Yahalom, M., Spitz, M., Sandler, L., Heno, N., Roguin, N., & Turgeman, Y. (2013). The Significance of Bradycardia in Anorexia Nervosa. International Journal of Angiology, 22(02), 083–094. https://doi.org/10.1055/s-0033-1334138