YASMIN ZAIDY
Gilberdyke Health Centre, Brough
Address for correspondence: Dr Yasmin Zaidy, GP Partner/Lifestyle Medicine Physician/Practice Diabetes and Obesity Clinical Lead, Gilberdyke Health Centre, Thornton Dam Lane, Brough HU15 2UL
E-mail: yasminzaidy@nhs.net
Br J Diabetes 2026;ONLINE AHEAD OF PUBLICATION
https://doi.org/10.15277/bjd.2026.502
Key words: Wernicke’s encephalopathy, GLP-1/GIP receptor agonist, tirzepatide, case report, optic neuropathy, thiamine deficiency
Wernicke’s encephalopathy (WE) is a neurological emergency most commonly associated with chronic alcohol misuse. However, it can also develop in individuals who are malnourished for reasons unrelated to alcohol, where timely diagnosis is often overlooked. WE has also been reported following bariatric surgeries such as Roux-en-Y gastric bypass and sleeve gastrectomy, particularly in patients with persistent vomiting and reduced oral intake. These procedures may increase risk by bypassing portions of the proximal small intestine, including the duodenum and jejunum, which are important sites of thiamine absorption.1,2 GLP-1/GIP receptor agonists are increasingly used in the management of diabetes and obesity. Although highly effective, these agents commonly cause appetite suppression and vomiting, which may predispose susceptible individuals to nutritional deficiencies and their associated complications.
A 49-year-old woman with a complex medical history, including type 2 diabetes (T2DM), overlap syndrome of autoimmune hepatitis (AIH) and primary biliary cholangitis (PBC), and iron-deficiency anaemia was treated with tirzepatide. Following an increase in her tirzepatide dosage, she began experiencing persistent vomiting and marked appetite suppression. She was subsequently admitted to hospital with vomiting and ketosis. During her hospital stay, she developed progressive neurological symptoms including drowsiness, confusion, difficulty walking, nystagmus and visual disturbances.
An MRI scan revealed characteristic signal changes consistent with WE, and she showed neurological improvement after commencing thiamine therapy. Despite early treatment ophthalmological assessment later revealed bilateral optic neuropathy. Psychiatric evaluation was conducted due to concerns regarding avoidant/restrictive intake patterns, but the patient did not report any psychological or emotional factors related to eating and opted not to pursue further mental health follow-up. Through a multidisciplinary inpatient rehabilitation programme, she experienced improvements in cognition, mobility and nutritional status.
This case highlights the growing safety considerations associated with GLP-1/GIP receptor agonists and the potential risk of non-alcoholic Wernicke’s encephalopathy in patients with multiple predisposing factors. While the temporal relationship with tirzepatide suggests a possible association, the presentation is likely multifactorial. The patient had a history of recurrent vomiting and probable underlying nutritional vulnerability, which may have contributed to the development of thiamine deficiency. These pre-existing factors, together with reduced oral intake, are likely to have increased the risk of Wernicke’s encephalopathy. Recent pharmacovigilance analyses have identified a safety signal for Wernicke’s encephalopathy with GLP-1 receptor agonists, including tirzepatide. Data from the FDA Adverse Event Reporting System (FAERS) indicate that Wernicke’s encephalopathy was disproportionately reported in association with semaglutide, tirzepatide and the GLP-1 receptor agonist class as a whole.3,4 Among reported cases, 68% occurred alongside symptoms such as nausea, vomiting or reduced food intake, with weight loss ranging from 3.5 to 13.3 kg per month over three to six months.3
While bariatric surgery protocols mandate structured nutritional monitoring, there are currently no equivalent frameworks in place for those receiving GLP-1RA therapy. Individuals using GLP-1 agonists for obesity management experience caloric reductions of 16%–39%.5 Such large, rapid reductions can result in inadequate intake of essential vitamins and minerals, particularly when energy intake falls below 1,200 kcal per day for females and 1,800 kcal per day for males.6 Observational studies have shown that those on GLP-1 therapy may develop nutritional deficiencies within 12 months, most frequently vitamin D, followed by thiamine and other B vitamins.7 A recent narrative review including 480,825 adults reported that micronutrient deficiencies may occur in patients receiving GLP-1 receptor agonist therapy. Vitamin D deficiency was the most common abnormality, affecting 7.5% of patients at six months and 13.6% at 12 months. Iron depletion was also frequently observed, with GLP-1 receptor agonist users demonstrating 26–30% lower ferritin levels compared with SGLT2 inhibitor users. Protein and calcium insufficiency were associated with lean mass loss, and deficiencies in thiamine and cobalamin increased over time.8
Wernicke’s encephalopathy is a medical emergency requiring prompt empirical thiamine therapy. Early thiamine supplementation should be considered in high-risk patients presenting with prolonged vomiting, significant weight loss or neurological symptoms even prior to imaging or laboratory confirmation. Empirical treatment dose is 500 mg intravenous thiamine (dissolved in 100 mL normal saline) infused over 30 minutes, three times daily for 2-3 days.9 In such cases, intravenous glucose should not be administered without concurrent thiamine replacement. IV glucose may aggravate acute thiamine deficiency and Wernicke's encephalopathy.10
Optic neuropathy is a rare but well-documented sequela of Wernicke’s encephalopathy. Classic ophthalmic manifestations include nystagmus, ophthalmoplegia and conjugate gaze palsies (occurring in approximately 29% of patients), but bilateral visual disturbances with optic disc oedema and retinal haemorrhages can be presenting features.9
The patient described her experience as frightening, especially given the sudden onset of cognitive and visual symptoms. She felt that her initial concerns were not fully acknowledged, resulting in distress due to delays in diagnosis. Nevertheless, she expressed gratitude for the support and care provided by the rehabilitation team. She continues to adapt to her ongoing visual impairment, reliance on walking aids, and difficulties with delayed memory recall. Motivated by her experiences, she is keen to raise awareness about the nutritional risks linked to medications such as tirzepatide.
This case highlights the potential for serious nutritional and neurological complications associated with GLP-1/GIP therapies, even in those without a history of alcohol misuse. Prompt recognition of Wernicke’s encephalopathy and admission to hospital for swift administration of thiamine are essential. The management of such complex cases involving chronic diseases necessitates a multidisciplinary approach.
© 2026. This work is openly licensed via CC BY 4.0.
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