Anorexia Nervosa (AN) is a serious eating disorder defined by extreme restriction of energy intake, leading to significantly low body weight and severe malnutrition. This profound state of starvation affects every major organ system, including the liver. Jaundice is characterized by the yellowing of the skin and the whites of the eyes. This discoloration occurs when there is a buildup of bilirubin, a pigment produced during the breakdown of red blood cells that the liver is responsible for processing and excreting. Severe AN can definitively cause jaundice, indicating a dangerous level of physical compromise.
Jaundice as a Sign of Severe Anorexia
The appearance of jaundice in a person with AN is a serious clinical finding that signals a medical emergency. While not common, its presence suggests the body has reached a state of profound energy deficiency and catabolism, where tissue breakdown exceeds repair. This symptom is a direct manifestation of severe liver dysfunction, often referred to as starvation-induced hepatitis, and is typically seen in severely malnourished individuals with a very low Body Mass Index (BMI).
True jaundice involves the yellowing of the sclera (the white part of the eye) and is a direct sign of hyperbilirubinemia, or elevated bilirubin in the blood. This must be distinguished from carotenemia, a less dangerous discoloration that causes a yellow-orange tint to the skin, particularly on the palms and soles. Carotenemia results from high levels of beta-carotene and does not affect the whites of the eyes.
How Starvation Impairs Liver Function
Severe malnutrition triggers physiological responses to conserve energy, fundamentally impairing the liver’s normal function. One primary mechanism is the development of hepatic steatosis, commonly known as fatty liver. Lacking dietary fuel, the body mobilizes fat stores, sending a large influx of free fatty acids to the liver for processing.
The liver cells, or hepatocytes, become overwhelmed and accumulate this fat, disrupting their internal cellular machinery. This excessive fat deposition impairs the liver’s ability to perform metabolic tasks, including the conjugation and excretion of bilirubin. This failure to properly process the pigment leads to its accumulation in the bloodstream, resulting in the visible yellowing of jaundice.
The state of extreme starvation also causes significant cellular stress and damage to the liver tissue, often termed “starvation hepatitis.” This involves the death and injury of hepatocytes, which release liver enzymes like aspartate aminotransferase (AST) and alanine transaminase (ALT) into the blood.
The severe lack of protein in the diet compromises the liver’s ability to synthesize necessary enzymes and transport proteins required for detoxification and efficient bilirubin processing. The combination of fat infiltration, cellular damage, and impaired enzyme function dramatically reduces the liver’s capacity to clear bilirubin from the circulation, resulting in clinically evident jaundice.
The Need for Immediate Medical Care
When jaundice is identified in a person with AN, immediate medical care and often hospitalization are mandatory. The symptom indicates severe organ stress and places the patient at high risk for serious complications, including acute liver failure. The primary therapeutic intervention is specialized nutritional rehabilitation, which must be carefully managed by a medical team.
The goal is to slowly reintroduce adequate nutrition to reverse the effects of starvation. Liver function typically improves rapidly once sufficient calories and nutrients are provided, often normalizing bilirubin levels within days or weeks. However, this process carries the risk of refeeding syndrome (RFS).
RFS occurs when a severely malnourished body suddenly shifts from a catabolic to an anabolic state. The sudden influx of carbohydrates stimulates insulin release, which drives electrolytes like phosphate, potassium, and magnesium into the cells. This causes dangerously low blood levels of these electrolytes, particularly hypophosphatemia, leading to cardiac, respiratory, or neurological failure. Therefore, the nutritional plan must be carefully titrated and monitored, with close attention paid to electrolyte levels.