Anorexia Nervosa (AN) is a serious psychiatric disorder defined by the restriction of energy intake, a significantly low body weight, and an intense fear of gaining weight. This extreme restriction forces the body into a state of chronic starvation, causing widespread medical complications and gastrointestinal distress. While AN may not cause a classic peptic ulcer, the physiological stress and malnutrition associated with the disorder profoundly compromise the entire digestive system.
Anorexia Nervosa and Direct Stomach Lining Damage
A traditional peptic ulcer is typically a deep sore caused by a bacterial infection (H. pylori) or the prolonged use of certain pain relievers. Anorexia Nervosa does not directly cause these types of ulcers. However, the physical effects of AN can lead to severe inflammation of the stomach lining, known as gastritis, which produces similar pain and discomfort. Chronic malnutrition deprives the stomach lining of the necessary nutrients to maintain its integrity.
The body’s stress response to starvation results in persistently elevated levels of the hormone cortisol. This chronic hypercortisolemia contributes to gastritis and compromises the gastric mucosal barrier. The compromised barrier, which normally protects the tissue from strong stomach acid, becomes vulnerable to erosion. These erosions and inflammation can mimic ulcer symptoms, such as burning pain in the upper abdomen, but they are distinct from deep peptic ulcers.
Other Common Gastrointestinal Functional Issues
Beyond direct mucosal damage, severe restriction in AN causes widespread functional issues as the body attempts to conserve energy. The lack of consistent food intake signals the digestive system to slow down, resulting in gastroparesis, or delayed gastric emptying. The muscles of the stomach and intestines weaken or atrophy due to underuse, and the nerves that regulate digestion, such as the vagus nerve, can become impaired.
Symptoms of gastroparesis include early satiety, nausea, vomiting, and a persistent feeling of fullness after eating only a small amount of food. Food can remain in the stomach for four hours or longer, roughly twice the normal emptying time. This digestive slowdown extends through the entire intestinal tract, which is the primary cause of chronic constipation.
Constipation is further exacerbated by the lack of physical bulk and fiber from restricted food intake, alongside chronic dehydration. Prolonged intestinal transit time means waste sits longer in the colon, allowing more water to be absorbed. This results in hard, dry stools that are difficult to pass.
Specific Damage Caused by Purging Behaviors
Specific compensatory behaviors, particularly self-induced vomiting and laxative abuse, cause distinct and severe gastrointestinal damage. Forceful or chronic vomiting creates a sudden, intense rise in pressure within the abdomen and esophagus. This pressure can cause a Mallory-Weiss tear, a mucosal laceration at the junction of the esophagus and the stomach.
These tears can lead to significant bleeding, often presenting as bright red blood in the vomit. Repeated exposure of the esophagus to stomach acid causes chemical erosion, leading to chronic acid reflux and esophagitis (inflammation of the esophageal lining). Laxative misuse primarily causes dangerous disturbances in fluid and electrolyte balance, particularly the loss of potassium and magnesium.
Electrolyte imbalance affects the electrical signaling needed for proper heart and nerve function. Prolonged use of stimulant laxatives causes colon dependence, leading to a condition sometimes described as a “lazy colon” where intestinal muscles lose their ability to contract naturally. This dependence can result in permanent loss of normal peristaltic activity and severe, refractory constipation.
Treating Gastrointestinal Complications During Recovery
The foundation for treating all gastrointestinal complications stemming from AN is nutritional rehabilitation and sustained weight restoration. Most functional issues, including gastroparesis and constipation, gradually improve and often resolve completely once normal eating patterns are established and the body is consistently nourished. This process requires careful medical oversight due to the risk of refeeding syndrome.
Refeeding syndrome is a potentially fatal complication characterized by severe, rapid shifts in fluid and electrolytes, such as hypophosphatemia, that occur when a severely malnourished person begins refeeding. To manage symptoms during early recovery, medical staff may use specific treatments. Gastroparesis symptoms are often managed through dietary modifications, such as consuming small, frequent meals low in fat and fiber, along with prokinetic medications like metoclopramide to stimulate gastric emptying.
For gastritis and esophagitis, acid-blocking medications, such as proton pump inhibitors or H2 blockers, are used to reduce irritation and allow the lining to heal. When treating constipation, non-stimulant methods like osmotic laxatives and stool softeners are preferred to gently restore bowel function, avoiding dependency risks associated with stimulant laxatives. Nutritional recovery is the ultimate remedy, allowing the digestive system’s muscles and nerves to regain strength and function.