Eating Disorders

"Eating disorders are serious illnesses marked by severe disturbances to one’s eating behaviors," and NIMH adds the two sentences families most need to hear: "Eating disorders are not a choice" — and "in some cases, they can be life-threatening. With treatment, however, people can recover from eating disorders." "The most common types of eating disorders include anorexia nervosa, bulimia nervosa, and binge eating disorder," and "Individuals may have more than one type of disorder."

Anorexia nervosa is "an eating disorder defined by restriction of energy intake relative to requirements, leading to a significantly low body weight. Patients will have an intense fear of gaining weight and distorted body image with the inability to recognize the seriousness of their significantly low body weight." In our own words, the DSM-5-TR criteria as summarized by Open RN are three: energy restriction leading to a significantly low weight for the person’s age, sex, development and health; an intense fear of weight gain or persistent behaviour that blocks weight gain despite the low weight; and a disturbed experience of body weight or shape — shape driving self-worth, or no recognition of how serious the low weight is. There are two subtypes, judged over the last three months. In the restricting type the person severely limits how much and what kind of food they eat, sometimes with excessive exercise; in the binge-eating/purging type there are episodes of binge eating and/or purging — self-induced vomiting or misuse of laxatives, diuretics or enemas. NIMH: people with anorexia nervosa "severely avoid or restrict food intake," and "Some people with anorexia nervosa may also have binge eating and purging episodes." One criterion students still memorise is gone: "Of note, amenorrhea has been removed from the DSM-5 criteria. Patients who meet the new criteria and continue to menstruate have similar outcomes as those who do not." And a patient can meet every criterion while sitting above a BMI of 18.5 — StatPearls calls this ‘atypical anorexia nervosa’. A normal weight does not rule out a dangerous eating disorder: "Even people who appear healthy can have eating disorders and be extremely ill."

Bulimia nervosa is binge eating followed by compensation: "Binge eating is followed by behaviors used to eliminate the excess food such as forced vomiting, excessive use of laxatives or diuretics, fasting, excessive exercise, or a combination of these behaviors." Restated in our own words, a binge is eating a clearly larger-than-normal amount in a discrete period — two hours is the example — with a sense of loss of control; binges and compensation both occur on average at least once a week for three months; self-evaluation is unduly driven by shape and weight; and it does not happen only during anorexia. The weight is the trap: "People with bulimia nervosa may be slightly underweight, normal weight, or overweight," so "Unlike anorexia nervosa, bulimia nervosa can be harder to detect." Where binges and purges happen only inside an anorexic illness, the diagnosis is anorexia, binge-purge type — "Clients with combination anorexia nervosa-bulimia nervosa have a significantly low body weight."

Binge eating disorder "is the most common eating disorder in the United States" — and "unlike bulimia nervosa, periods of binge eating are not followed by purging, excessive exercise, or fasting. As a result, people with binge eating disorder often are overweight or obese." In our own words: binges with loss of control, at least weekly for three months, with marked distress and at least three of five features — eating very fast, eating until uncomfortably full, eating large amounts without hunger, eating alone out of embarrassment, and disgust, depression or guilt afterwards — and no regular compensation. Severity is graded by the number of binge episodes a week (mild 1–3, moderate 4–7, severe 8–13, extreme 14 or more). The behavioural difference from bulimia is precise: "Patients with bulimia nervosa typically restrict their diet between binge eating episodes to influence their body shape. In contrast, those with binge eating disorder do not limit their intake in between events." Two further diagnoses are named only for recognition: ARFID, where "people with ARFID do not have a distorted body image or extreme fear of gaining weight," and pica — "Pica refers to chronic ingestion of nonfood substances and may be a manifestation of underlying medical or psychiatric condition" (StatPearls).

The biology is real, and it is about reward and control circuits rather than appetite alone. In anorexia "there are deficits in neurotransmitters dopamine (eating behavior and reward) and serotonin (impulse control and neuroticism), differential activation of the corticolimbic system (appetite and fear), and diminished activity among the frontostriatal circuits (habitual behaviors)." Open RN describes how the illness locks itself in: "For those genetically vulnerable to eating disorders, initial weight loss may reinforce a reward feedback mechanism and establish a maladaptive eating behavior pattern. Physiological and sensorial changes result in alterations in hunger and satiety, gastrointestinal motility, and decision-making around food and eating." In bulimia, "The abnormalities in interoceptive function, particularly of the insula, may contribute to the binging behavior."

The psychological core is control, which is why trust comes before food. Clients with anorexia "value their obsessive-compulsive behaviors with eating as a way to feel safe and secure and avoid negative feelings," and "Their relationship with food is not merely about nutrition but is often deeply tied to control, self-worth, identity, or coping with distress." That is the physiology behind the first nursing priority on this page. In bulimia and binge eating disorder the engine is a loop: "Over-evaluating body shape and weight produces dysfunctional eating and dieting behavior, which in turn causes physiological and psychological vulnerability to episodes of binge eating," and "Awareness of binge episodes and knowledge of strategies for self-control help prevent the cycle of binging and guilt."

Genes load the gun; the environment points it. "Eating disorders are hereditary." But "Although genetics increases the risk for developing eating disorders, the individual’s environment plays a significant role," and the disorders "commonly start in adolescence and young adulthood when there can be exceptional pressure from peers, social media, advertisements, etc., to diet or lose weight." Sport is a named pressure — wrestling, gymnastics, figure skating and body building in one source; ballet, long-distance running and martial arts in another. Binge eating disorder has "a heritability estimate of 41% to 57%."

In anorexia the damage comes from starvation; in bulimia it comes from the method. "Unlike in anorexia nervosa, in which complications are due to weight loss and malnutrition, the type and severity of medical complications of bulimia nervosa can be determined based on the frequency and the method the patient uses to purge." Starvation produces the slow, visible picture — bradycardia, hypotension, cold intolerance, lanugo, constipation, amenorrhea, osteopenia, anemia. Purging produces the fast, invisible one.

Vomiting throws away acid, fluid and potassium, and that is the chain to draw. "Laboratory abnormalities associated with bulimia nervosa include hypokalemia (including hypokalemic hypochloremic metabolic alkalosis), hyponatremia, and transaminitis," and "The most common cause of metabolic alkalosis in patients with bulimia nervosa is fluid volume depletion." Laxative misuse can shift the acid–base picture the other way, while diuretic misuse, like vomiting, causes alkalosis — StatPearls lists "hypokalemic metabolic acidosis or alkalosis (laxative or diuretic abuse, resp.)." The endpoint is the heart: "Cardiac arrhythmia - can be caused by hypokalemia due to self-induced vomiting. Hypokalemia can contribute to QTc prolongation." Open RN states the priority plainly: "Electrolyte disturbances (especially hypokalemia) are life-threatening and common with vomiting, laxative use, and restriction," and "Early detection is critical to prevent sudden cardiac arrest."

The visible signs of purging are the clues to a hidden behaviour. Russell’s sign — "calluses on the dorsal aspect of the hand" — comes from self-induced vomiting. "Dental enamel erosion - result from gastric acid washing over teeth." Open RN lists parotid swelling with increased serum amylase levels. Vomiting also "lowers seizure threshold," and ipecac abuse "is associated with other cardiac complications, including congestive heart failure and death." Laxatives do not even achieve their purpose — they "work in the gastrointestinal tract after the areas where caloric absorption has occurred primarily."

"Refeeding syndrome is defined as medical complications that result from fluid and electrolyte shifts as a result of aggressive nutritional rehabilitation." It happens because starvation has quietly emptied the cells: "starvation increases gluconeogenesis and proteolysis. In contrast, metabolic substrates, including vitamins and intracellular electrolytes, are depleted." Serum values can look acceptable while total-body stores are gone. Who is at risk is stated simply: "Any client with negligible food intake for more than five days is at risk of developing a potentially fatal complication called refeeding syndrome."

Then food arrives and insulin moves everything into the cells at once. "Sudden initiation of nutritional replenishment following extended periods of starvation results in rising glucose levels in the bloodstream. With rising glucose levels, the body produces a countermeasure that increases insulin levels, which then drive phosphorus and potassium intracellularly, causing a decrease in the amount of available extracellular potassium or hypokalemia." Phosphate is then consumed as the cells start making energy: "As the body utilizes glucose to produce molecules of adenosine triphosphate (ATP), it depletes the remaining stores of phosphorus." Hence the hallmark: "Hypophosphatemia is a hallmark of refeeding syndrome; however, other electrolyte irregularities may include but are not limited to decreased amounts of magnesium, potassium, and thiamine."

Each missing electrolyte has a lethal endpoint. "Low levels of phosphorous are linked to decreased cardiac contractility and arrhythmias, which could be fatal," and low 2,3-DPG causes "a leftward shift in the oxygen-hemoglobin dissociation curve, increasing hemoglobin’s affinity for oxygen and decreasing oxygen release to the tissues" — "in severe cases, hypophosphatemia can lead to acute respiratory failure." "Hypokalemia may lead to cardiac arrhythmias or weakness, fatigue, paralysis, hypoventilation and respiratory distress." Low magnesium "can exacerbate hypokalemia and increase renal potassium wasting," and together they "may equally contribute to torsades de pointes." Thiamine needs rise sharply with feeding, so deficiency can tip into Wernicke’s encephalopathy — "memory impairment, ophthalmoplegia, ataxia." The history is sobering: "In 1951, Schnitker et al reported that one-fifth of Japanese prisoners starved in prison camps died suddenly after nutritional and vitamin replenishment."

ASPEN defines it by how far the electrolytes fall, and when. Refeeding syndrome is "a decrease in any 1, 2, or 3 of serum phosphorus, potassium, and/or magnesium levels by 10%-20% (mild), 20%-30% (moderate), or >30% and/or organ dysfunction resulting from a decrease in any of these and/or due to thiamin deficiency (severe), occurring within 5 days of reintroduction of calories." That is why the nurse compares each result with the patient’s own baseline, not only with a reference range. The earliest cue is subjective: "Clinically, it has been observed that a patient’s first described feeling of nausea can be interpreted as a precursor to hypotension."