Atypical anorexia after weight loss

A 2026 case report describes a woman who developed atypical anorexia nervosa after sleeve gastrectomy followed by treatment with semaglutide and then tirzepatide. Her weight fell from 113 kg before surgery to 50.3 kg three years later. The report cannot show that either medicine caused the eating disorder. Clinicians assessing rapid weight loss need information about fear of weight gain, restrictive eating, and signs of malnutrition as well as body mass index^[1].

The clinical course

The patient was a 60-year-old Japanese woman with type 2 diabetes and a long history of depression and disordered eating. Before surgery, she weighed 113 kg and had a BMI of 47.0. She underwent laparoscopic sleeve gastrectomy at age 57. Semaglutide was restarted one month later because of diabetes and her wish to lose more weight. After one year, she weighed 73 kg. She then requested a medicine with a stronger weight-loss effect, and treatment changed to tirzepatide^[1].

The tirzepatide dose was gradually increased during care. The clinical team set a target weight of 60 kg and later reduced the dose as she approached it. Three months before admission, her appetite fell sharply and edema appeared. Her endocrinologist recommended stopping tirzepatide, but she continued it. She wanted to weigh less than 48 kg, restricted her intake to 600 to 800 calories a day without carbohydrates, and remained intensely afraid of gaining weight^[1].

At admission, she weighed 50.3 kg and had a BMI of 20.9. Laboratory and examination findings included systemic edema, a serum albumin level of 2.8 g/dL, hemoglobin of 9.7 g/dL, and low body fat. These were clinical signs of malnutrition despite a BMI above the usual underweight threshold. A psychiatrist assessed her fear of weight gain, body-image preoccupation, restricted intake, and limited recognition of the seriousness of her condition^[1].

Why the diagnosis was atypical anorexia

Atypical anorexia nervosa describes people who meet the psychological and behavioral criteria for anorexia nervosa but whose weight remains in the normal or higher range after substantial loss. In this case, the team documented energy restriction, intense fear of weight gain, persistent behavior that interfered with weight gain, and poor recognition of the medical danger. Her BMI remained above 18.5, so the diagnosis was atypical rather than classic anorexia nervosa^[1].

The label can be easy to miss after obesity treatment. Weight loss may still be praised even when eating has become rigid and the patient is medically unwell. BMI alone did not capture the risk here. The edema, anemia, low albumin, severe restriction, fear of weight gain, and continued pursuit of a lower weight supplied the more useful picture.

Treatment and early recovery

The hospital stopped tirzepatide and treated the malnutrition with inpatient nutritional care. The paper reports a supervised 1,800-calorie diet and 70 to 90 grams of protein per day, not advice for readers. After one month, her weight had risen to 60 kg, albumin to 3.8 g/dL, and hemoglobin to 11.7 g/dL. Outpatient psychiatric care included supportive psychotherapy, education about eating-disorder risks, and regular follow-up. The authors report that her fear of fatness and guilt after eating became less intense^[1].

Stopping appetite-suppressing treatment addressed only one part of the problem. The patient also had longstanding depression, earlier binge eating, major life stress, pressure from partners to lose weight, and a fixed belief about the weight she should reach. Her care involved endocrinology, surgery, nutrition, and psychiatry.

What the report can and cannot show

This is one case report. There was no comparison group, and sleeve gastrectomy, semaglutide, tirzepatide, psychiatric history, social pressure, and the patient's own drive for further loss overlapped. The authors therefore describe the surgery and medicines as possible triggering or contributing factors. They do not establish that semaglutide or tirzepatide independently caused atypical anorexia nervosa^[1].

The sequence also deserves care. Semaglutide started one month after surgery, treatment later changed to tirzepatide, and the eating disorder was diagnosed three years after surgery. The paper calls this the first reported case with this specific combination and timing. A first report is a clinical warning signal, not an estimate of frequency or proof that the same outcome is likely for other patients^[2].

The authors also describe several vulnerabilities that existed before the medicines were used. Depression began decades earlier, disordered eating preceded surgery, and personal relationships reinforced the pressure to lose weight. The report does not separate the effect of any one factor. Larger studies would be needed to measure how often restrictive eating develops after bariatric surgery with or without incretin treatment^[1].

Why this matters for follow-up

Follow-up after major weight-loss treatment should include behavior and mental health, not only kilograms, glucose, and BMI. A normal BMI does not rule out serious restriction or malnutrition. New fear of weight gain, a rigid target weight, avoidance of food, continued weight-loss efforts despite physical decline, edema, weakness, or abnormal blood tests warrant clinical assessment.

For readers using prescription incretin medicines, the practical point is not to change treatment alone. Rapid or unexpected loss and a strained relationship with food should be discussed promptly with the prescribing clinician. Our tirzepatide evidence page and semaglutide evidence page explain the medicines and their established trial evidence. This case adds a narrower lesson: medically dangerous restriction can develop even when the scale does not show an underweight BMI.