Two common GLP-1 weight loss drugs have been linked to a brain condition that can cause permanent brain damage and become deadly.
More than one in 10 American adults are now on GLP-1s for weight loss. And while the jabs work to shed pounds and provide a host of other unexpected benefits, they can come at a cost.
GLP-1s work by slowing down digestion, making us feel full for longer. The resulting decrease in appetite and food intake can lead to inadequate nutrition, including a deficiency in vitamin B1, also known as thiamine.
This essential vitamin helps the brain produce energy. Without enough of it, brain cells can’t function properly, potentially leading to Wernicke 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 people using GLP-1s could be more likely to develop a vitamin B1 deficiency — and, in turn, WE.
Their findings identified two GLP-1 meds in particular that could increase the risk of this condition.
What researchers found
Researchers examined 195,979 cases and identified 15 cases of Wernicke’s encephalopathy.
They found that WE disproportionately associated with GLP-1s compared with other drugs. Most of the cases involved two medications in particular: semaglutide, sold as Ozempic, Wegovy, and Rybelsus, and tirzepatide, sold as Mounjaro and Zepbound.
The researchers highlighted that most of the patients with WE experienced gastrointestinal issues, including weight loss, vomiting, loss of appetite or malnutrition, all of which can contribute to inadequate nutrition and vitamin B1 deficiency.
Only two of the patients exhibited that signature triad of WE symptoms — altered mental state, trouble walking, and lack of control over eye movements — highlighting how difficult the condition can be to recognize.
While the findings underscore that WE is a “potentially rare” adverse event, the researchers urged clinicians to look out for the condition, particularly in patients taking semaglutide or tirzepatide, to help prevent permanent brain damage and save lives.
What is Wernicke encephalopathy?
Wernicke encephalopathy is caused by a severe vitamin B1 deficiency. The vitamin is essential for helping brain cells produce energy. Without enough of it, brain cells can’t function properly, leading to inflammation and swelling in regions of the brain responsible for memory and balance.
That damage can cause the signature triad of WE symptoms, but only 10% to 16% of people with WE exhibit the all three signs, making it difficult to distinguish from conditions such as dementia or intoxication.
As a result, most cases — as many as 80% — go undiagnosed. Some are only identified after death, during autopsy.
WE is treatable if caught early. Giving patients the vitamin B1 they’re missing, often through an IV, can help stop the damage from progressing.
But the stakes are high: Without treatment, WE can quickly become fatal in up to 20% of cases, and as many as 85% of survivors develop permanent brain damage.
Who else is at risk?
WE is most commonly associated with chronic alcoholism. Over time, drinking can cause gut inflammation, making it harder for the body to absorb vitamin B1. Alcohol also hurts the liver’s ability to store the vitamin.
The condition has also been linked to bariatric surgery, which can decrease nutrient absorption.
A teen who experience cannabinoid hyperemesis syndrome aka CHS or “scromitting” — a condition in which too much marijuana consumption leads to repeated vomiting — developed a B1 deficiency and WE.
And what if that critical nutrient never gets into the body to begin with?
Anorexia, a condition in which people may severely restrict food intake to control their weight, has also been linked to WE.
