Anorexia Nervosa (AN) is classified as a psychiatric disorder, but its defining characteristic is chronic starvation and malnutrition, which causes severe physical complications. The gastrointestinal (GI) system is highly sensitive to nutritional status. As a direct consequence of chronic restricted intake and severe weight loss, AN causes significant stomach and other GI issues. These digestive problems result from physiological changes that affect the entire alimentary canal, often becoming a major hurdle in the path toward recovery.
The Impact of Starvation on Digestive Motility
Long-term caloric restriction forces the digestive system into a state of severe underuse, which dramatically slows the movement, or motility, of the entire gastrointestinal tract. This slowdown is primarily a mechanism of energy conservation, as the body attempts to extract every possible calorie from minimal food consumed. The smooth muscles lining the stomach and intestines begin to weaken and lose tone, similar to how skeletal muscles atrophy from disuse.
This loss of muscle tone often leads to gastroparesis, a condition defined by delayed stomach emptying. In AN patients, food can remain in the stomach for up to twice as long as in a healthy individual. The reduced volume of food provides insufficient mechanical stimulus for the stomach muscles to contract efficiently. This further exacerbates the sluggish transit time and perpetuates the cycle of delayed emptying.
The problem extends beyond the stomach to the lower GI tract, resulting in chronic constipation. This common complaint is caused by severe dehydration, lack of sufficient dietary fiber, and a significantly slowed colonic transit time. Waste elimination becomes impaired as the body’s metabolic rate slows down to conserve resources.
Motility issues are regulated by the nervous system and hormones, both of which are profoundly affected by starvation. The autonomic nervous system, which controls involuntary bodily functions like digestion, exhibits dysregulation in AN. Hormonal signals governing hunger and satiety are also altered, such as the elevation of ghrelin, the appetite-stimulating hormone. This high level of ghrelin is likely an adaptive physiological response to critically low energy stores, rather than a driver of increased appetite.
Physical Consequences and Tissue Vulnerability
The slowed movement of the digestive tract leads to specific, distressing physical consequences that complicate the patient experience. Severe bloating and distension are nearly universal complaints, often occurring even after consuming a very small meal. This experience of early satiety is a direct manifestation of gastroparesis, as the stomach is still physically full from the previous, slowly emptying meal. The bloating sensation is often paradoxical, resulting from sluggish movement causing gas buildup and an uncomfortable feeling of fullness.
Anatomical changes due to extreme weight loss pose a risk of structural complications. In cases of severe fat and muscle depletion, the protective fat pad between the aorta and the superior mesenteric artery (SMA) can disappear. This anatomical shift can compress the duodenum, the first part of the small intestine, leading to Superior Mesenteric Artery (SMA) Syndrome. This partial intestinal obstruction causes severe abdominal pain, nausea, and vomiting, further hindering nutritional intake.
A more acute risk is Acute Gastric Dilation (AGD), which occurs when the severely weakened and atrophied stomach wall is suddenly confronted with a large volume of food. This can happen during a binge episode or during the initial stages of aggressive refeeding. The muscle atrophy prevents the stomach from contracting or emptying, causing extreme dilation that risks gastric necrosis, perforation, and shock. AGD is a medical emergency requiring immediate intervention, highlighting the vulnerability of the starved digestive tissues.
In patients who engage in self-induced vomiting, the esophagus is susceptible to severe irritation and damage. Frequent exposure to stomach acid can cause painful esophageal inflammation (esophagitis) and chronic acid reflux (GERD). Forceful vomiting can also result in a Mallory-Weiss tear, a longitudinal laceration of the mucous membrane at the junction of the esophagus and stomach. These tears can lead to significant upper gastrointestinal bleeding and are a serious complication of purging behaviors.
Management and Recovery of Gastrointestinal Function
The primary treatment for nearly all gastrointestinal dysfunction caused by Anorexia Nervosa is sustained nutritional rehabilitation and weight restoration. The majority of motility and functional issues, including gastroparesis and chronic constipation, are reversible as the body receives consistent nourishment and returns to a healthy weight. Recovery is gradual, however, and symptoms often worsen temporarily during the initial refeeding phase as the body’s digestive capacity slowly adapts.
Managing gastroparesis symptoms often involves specific dietary adjustments designed to ease the digestive load. Patients are advised to consume smaller, more frequent meals throughout the day, which helps prevent excessive stomach distension and reduces the feeling of fullness. The diet is often temporarily modified to be low in fat and fiber, as both macronutrients slow gastric emptying of solids, intensifying delayed transit symptoms.
Medical supervision is necessary during refeeding to monitor for acute complications like AGD and to mitigate the risks associated with Refeeding Syndrome, a dangerous metabolic shift involving severe electrolyte abnormalities. When gastroparesis is severe and significantly impedes the ability to eat, prokinetic medications may be used short-term to stimulate muscle movement. Metoclopramide is one such agent that works by blocking dopamine receptors and increasing acetylcholine levels, encouraging the stomach to empty faster. Due to the risk of neurological side effects like tardive dyskinesia, this medication is reserved for severe cases and prescribed for a limited duration.