A new study has revealed that popular GLP-1 weight-loss drugs may increase the risk of vitamin B1 deficiency, which can cause permanent brain damage and even death.
The researchers identified two specific drugs, semaglutide and terzepatide, that are disproportionately associated with this condition.
GLP-1 drugs work by slowing down digestion, making us feel full for longer. This decreased appetite and reduced food intake can lead to inadequate nutrition, including a deficiency in vitamin B1 (thiamine), an essential vitamin that helps the brain produce energy. Without enough thiamine, brain cells cannot function properly, potentially leading to Wernicke's encephalopathy (WE), a rare but serious neurological disorder that can cause permanent brain damage or death if left untreated.
Researchers in Israel suspected that many GLP-1 users might be more susceptible to vitamin B1 deficiency and, consequently, Wernicke's encephalopathy. They examined 195,979 cases and identified 15 instances of this condition, finding it disproportionately associated with GLP-1 medications compared to other drugs.
semaglutide (marketed under several trade names that vary according to the therapeutic purpose and dosage: Ozempic, Yegovi, Rebelsus) and terzipatide (Mangaro, Zipound).
The researchers noted that most patients suffered from gastrointestinal problems, such as weight loss, vomiting, loss of appetite, or malnutrition, all of which can contribute to vitamin B1 deficiency. Only two patients exhibited the characteristic triad of symptoms of Wernicke's encephalopathy—altered mental status, difficulty walking, and loss of control over eye movements—highlighting the difficulty in identifying this condition.
Although the results confirm that Wernicke's encephalopathy is a "rare" adverse event, the researchers urged doctors to monitor it, especially in patients taking semaglutide or terzepatide, to prevent permanent brain damage and save lives.
This condition is caused by a severe deficiency of vitamin B1, leading to inflammation and swelling in brain regions responsible for memory and balance. Although the condition has three characteristic signs, only 10% to 16% of those affected exhibit all three, making it easily mistaken for dementia or poisoning. For this reason, most cases—up to 80%—remain undiagnosed, and some are only discovered after death.
Wernicke's encephalopathy is treatable if detected early, with patients receiving the missing vitamin B1, often intravenously, to halt the progression of the damage. However, the risks are high: without treatment, it can be fatal in up to 20% of cases, and up to 85% of survivors suffer permanent brain damage.
Wernicke's encephalopathy is commonly associated with chronic alcoholism, causing inflammation in the intestines and impairing the liver's ability to store vitamins. It has also been linked to bariatric surgery, which reduces nutrient absorption, as well as to cannabis-associated hyperemesis gravidarum (CHS) and anorexia nervosa.
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