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Kevin Chen, MD, ScM; Patrick Ho, MD, MPH; and Eduardo Andres Calagua-Bedoya, MD

Published: November 14, 2024

Anorexia nervosa (AN) is the second most lethal psychiatric disorder behind substance use disorders.1 Patients with comorbid AN and alcohol use disorder (AUD) have 10 times the risk of mortality compared to patients without AUD.1 Patients with AN have an increased risk of developing AUD2: 1 in 5 patients with any eating disorder will abuse alcohol in their lifetime.3 In this report, we highlight associations between AN and AUD, emphasizing biological and psychological aspects of both conditions.

Ms D is a 57-year-old woman with a medical history of osteoporosis, headaches, gastroesophageal reflux disease, irritable bowel syndrome, major depressive disorder, AN, anxiety, and AUD. She was referred from neurology for outpatient psychiatric consultation given her complex psychiatric history.

Ms D describes disordered eating behaviors including food avoidance and restriction, with compensatory behaviors such as self-induced vomiting; use of laxatives, diuretics, and enemas; and extreme exercise. Her eating problems stem from early childhood experiences revolving around control and sibling rivalry. Although her current body mass index is 15 kg/m2, she continued to weigh herself daily, believing she was overweight. She also reports neurovegetative symptoms of depression, comorbid anxiety, and history of abuse but denies trauma related symptoms. Ms D began using alcohol in college but then transitioned to daily alcohol use in her 40s. She continues to use alcohol on a daily basis to stimulate her appetite.

Complete blood count, comprehensive metabolic panel, thyroid function tests, vitamin levels, and estradiol parameters are all within normal range, but her lipase level is increased. Recent brain magnetic resonance imaging with and without contrast revealed evidence of a remote ischemic event in the frontal area with no acute anomalies, and cortical volume is age appropriate. The psychiatry team recommended that Ms D transition from paroxetine to fluoxetine and initiate olanzapine to target insomnia, poor appetite, impulsivity, and depression. She declined medications for AUD or referrals to eating disorder programs.

After a subsequent follow-up with her primary care provider, olanzapine was initiated, and she was advised to decrease her alcohol intake. She declined to start fluoxetine, fearing side effects and hepatotoxicity, instead opting to continue paroxetine. She initially reported benefit from olanzapine, though subsequently self-discontinued it after reporting insomnia and palpitations. She ultimately elected to transfer care to her local community mental health center to access more comprehensive psychiatric care.

AN and AUD share several biological and psychological features. As an example, both entities can exhibit cardiac dysfunction.4,5 Likewise, given their underlying deficits in oral intake, patients with AN and AUD are prone to hypokalemia and hypomagnesemia, which can lead to QTc prolongation and subsequent limitations in the use of psychotropic agents.6 Other biopsychological characteristics seen in both disorders are described in Table 1. These include genetic aspects,7 alterations in the endocannabinoid8–10 and brain reward systems,6,11–16 nutritional deficiencies,17–20 character traits,6,21 intrapsychic conflicts,22 defense mechanisms,23,24 and cognitive distortions.25,26 A clear illustration of the psychological complexities seen in both AUD and AN was the degree of cognitive dissonance present in this patient: she considered herself to be overweight, but she also used alcohol to stimulate her appetite—the natural outcome of an increase in appetite is weight gain, which was also her biggest fear. Noteworthy, as subjects with AN and AUD suffer from complex medical comorbidities,4,5,19,20 routine monitoring of side effects is advised when prescribing psychotropic agents. The patient described here tried different antidepressants and antipsychotics for her symptoms, including medications that had been utilized years before our initial encounter with her. The advantages and disadvantages27–31 of these specific agents when treating individuals with AN and AUD are delineated in Table 2.

AN and AUD share similar etiologic factors. Exploration of biologic, psychodynamic, and cognitive behavioral aspects in AN and AUD is key for treatment purposes. Comorbid AN and AUD carry a poor prognosis, and pertinent screenings should be in place when providing care to these populations.32 Patients with comorbid AN and AUD may benefit from a multimodal treatment approach involving pharmacotherapy and psychotherapy. When feasible, both entities should be treated concurrently. Several interventions have evidence for both AN and AUD such as self-help approaches, cognitive-behavioral therapy, psychodynamic psychotherapy, dialectical behavior therapy, family and couples therapy, and motivational interviewing.32 Psychiatrists, especially those working in embedded/collaborative care settings, can assist with diagnosing and treating these comorbid conditions. Treatments for both AN and AUD are individualized and must take into consideration each patient’s intrinsic motivation and readiness for change.

Published Online: November 14, 2024. https://doi.org/10.4088/PCC.24cr03806
© 2024 Physicians Postgraduate Press, Inc.
Prim Care Companion CNS Disord 2024;26(6):24cr03806
Submitted: July 3, 2024; accepted August 29, 2024.
To Cite: Chen K, Ho P, Calagua-Bedoya EA. The comorbidity between eating disorders and alcohol misuse: biological and psychological perspectives illustrated by a case report. Prim Care Companion CNS Disord. 2024;26(6):24cr03806.
Author Affiliations: Department of Psychiatry, Dartmouth Hitchcock Medical Center, Lebanon, New Hampshire (all authors).
Corresponding Author: Eduardo Andres Calagua-Bedoya, MD, Department of Psychiatry, Dartmouth Hitchcock Medical Center, One Medical Center Drive, Lebanon, NH 03756 ([email protected]).
Relevant Financial Relationships: None.
Funding/Support: None.
Previous Presentation: Poster presented at the 2024 APA Annual Meeting; May 4–8, 2024; New York, New York.
Patient Consent: Consent was received from the patient to publish the case report, and information has been de identified to protect patient anonymity.