Anorexia Nervosa (AN) is a serious eating disorder characterized by severe food restriction, an intense fear of gaining weight, and a distorted body image. Diabetes Mellitus (DM) is a chronic metabolic disorder where the body cannot properly regulate blood sugar (glucose) due to issues with the hormone insulin. While AN does not typically cause diabetes, the profound malnutrition significantly alters the body’s metabolic function. This disruption creates a complex relationship that can increase the risk of developing Type 2 Diabetes (T2D) later in life or severely complicate the management of pre-existing Type 1 Diabetes (T1D).
How Anorexia Affects Acute Glucose Metabolism
Severe caloric restriction forces the body to dramatically change how it produces energy. The body first depletes its stored sugar reserves, known as glycogen, primarily located in the liver and muscles. Once reserves are gone, the body enters starvation, initiating gluconeogenesis, where it creates new glucose from non-carbohydrate sources like fat and muscle protein.
This sustained low energy intake often leads to hypoglycemia (abnormally low blood sugar), which can be a dangerous complication in advanced AN cases. In response to the persistent lack of incoming fuel, the body decreases its production of insulin. This is an appropriate metabolic adaptation to prevent blood sugar from dropping too low.
A paradoxical effect, “starvation-induced pseudo-diabetes,” can emerge during the acute refeeding phase. When carbohydrates are reintroduced, the body’s insulin response can be delayed or decreased. This temporary impaired glucose tolerance occurs because the body is overwhelmed by sugar while its metabolic machinery is still operating in starvation mode. This shift, combined with electrolyte disturbances, is a risk factor for the life-threatening condition known as refeeding syndrome.
Anorexia and the Risk of Developing Type 2 Diabetes
The long-term metabolic consequences of Anorexia Nervosa can increase the risk of developing Type 2 Diabetes (T2D) years after the acute phase has passed. This risk is linked to the chronic stress and recovery process, not the initial starvation. Chronic psychological stress associated with the eating disorder can lead to elevated levels of the stress hormone cortisol. High cortisol contributes to insulin resistance, a condition where the body’s cells stop responding effectively to insulin, which is the precursor to T2D.
Weight cycling, the pattern of losing and regaining weight during and after recovery from AN, also burdens the metabolic system. During weight restoration, the body may preferentially accumulate fat around internal organs, known as visceral adiposity. This visceral fat is metabolically active and strongly linked to the development of insulin resistance.
Insulin resistance may persist even after an individual has achieved a fully restored weight. The long-term stress placed on the pancreas and metabolic system during cycles of starvation and refeeding impairs the body’s ability to manage glucose effectively. The metabolic strain from Anorexia Nervosa creates a vulnerability that can manifest as T2D later in life.
The Unique Challenge of Type 1 Diabetes and Anorexia
The co-occurrence of Type 1 Diabetes (T1D) and Anorexia Nervosa presents a distinct and dangerous clinical challenge. T1D is an autoimmune condition where the body cannot produce insulin, and it is not caused by the eating disorder. However, individuals with T1D are at a significantly increased risk of developing an eating disorder.
Managing T1D requires constant monitoring of food intake and strict insulin dosing, which can heighten preoccupation with food and body weight. A severe behavior known as “Diabulimia,” or ED-DMT1, occurs when a person with T1D intentionally restricts or omits insulin to manipulate their body weight. Insulin is an anabolic hormone, and when taken as prescribed, it can lead to weight gain, which a person with AN often fears.
Restricting insulin prevents the body’s cells from using glucose for energy, forcing the body to break down fat and muscle mass for fuel, leading to weight loss. This intentional insulin deficiency causes severe hyperglycemia (high blood sugar) and a buildup of toxic acidic compounds called ketones. This quickly leads to Diabetic Ketoacidosis (DKA), a medical emergency that can result in coma or death. The long-term consequences of chronic high blood sugar from insulin omission include the accelerated onset of severe microvascular complications, such as damage to the kidneys, eyes, and nerves.
Treatment and Recovery for Dual Diagnoses
Successfully treating an individual with a dual diagnosis requires a highly specialized and integrated approach. A multidisciplinary care team is necessary, typically involving endocrinologists, mental health specialists, and registered dietitians. The conditions must be managed simultaneously, as addressing one without the other is often ineffective and dangerous.
Insulin management, particularly for those with T1D, requires a careful balance to prevent both dangerous hypoglycemia during refeeding and intentional insulin omission. Psychological treatment focuses on the underlying mental health issues, such as body image distortion and the need for control. Nutritional rehabilitation must be closely monitored to ensure weight restoration and stable blood sugar control while addressing the psychological components of the eating disorder.