GLP-1 Medications: A New Option for People Living with IBD?
- Sheila Thompson, RN CPHQ
- 26 minutes ago
- 4 min read
Ozempic, Wegovy, Moujaro, Zepbound…these medications have been all over the media as the latest trend in weight loss drugs, but did you know they were developed for another purpose?
What are GLP-1 agonists?
Glucagon-like peptide 1 (GLP-1) is a naturally occurring human hormone. When a person eats or drinks, the body responds by releasing GLP-1 from the small intestine. This triggers the pancreas to release insulin while suppressing the release of glucagon, slows gastric emptying, and decreases hunger by helping one feel full.
People with type 2 diabetes may not respond to GLP-1 adequately or at all, so introducing a GLP-1 agonist helps the body’s GLP-1 receptors recognize and use the hormone more effectively. Also known by generic names such as semaglutide and tirzepatide, these medications function as GPL-1 agonists, meaning they are manufactured substances that mimic naturally occurring ones. They are dose dependent, so higher doses have stronger effects. They were first approved in 2005 to treat people with type 2 diabetes, causing lower blood sugar and beneficial weight loss. GLP-1 agonists have become an important tool in diabetes management, alongside exercise, lifestyle and diet changes, and other medications such as metformin.
Because GLP-1 agonists are so effective in contributing to significant weight loss, the FDA approved some of them to treat obesity, defined as a body mass index (BMI) of 30 or greater, even in people who don’t have diabetes. A healthcare practitioner may also include these medications in a person’s treatment plan if they are overweight (BMI of 25 to 29.9) and have another coexisting condition that may improve with weight loss.
What is Inflammatory Bowel Disease?
Researchers noted various similar hormone receptors in the human body and began to explore the potential impact of GLP-1s on other organ systems and the inflammatory process. Inflammatory Bowel Disease (IBD), including ulcerative colitis and Crohn’s disease, are thought to develop due to inflammation and improperly regulated immune responses in genetically predisposed individuals. These life-long chronic diseases affect millions worldwide, causing symptoms such as abdominal pain and cramping, bloody stool, diarrhea, and fatigue. Over time, the individual may experience periods of disease activity (“flares”) and of remission. Management may include avoiding triggers such as smoking, stress, and certain medications. Drinking beverages containing milk, caffeine, or carbonation, and eating foods containing a lot of fiber or grease, may make symptoms worse but aren’t thought to cause symptoms.
IBD can cause a variety of complications, including malabsorption and malnutrition, unintended weight loss, kidney stones, anemia, mouth sores, skin rashes, eye irritation, swollen joints, osteoporosis, and liver disease. Treatment may include medications such as antidiarrheals, corticosteroids for inflammation, immunosuppressants, and biologics, which can help calm the immune response. In extreme cases, a person with IBD may develop fistulas (abnormal connections between organs or an organ and the skin’s surface), strictures or stenosis (narrowing of the intestine), intestinal perforations, toxic megacolon, or colon cancer. Hospitalization may be necessary if the person becomes severely dehydrated, anemic, or malnourished, and surgical intervention may be needed to treat fistulas, strictures, perforations, and other serious complications.
What is the connection between GLP-1 agonists and IBD?
Various studies have identified higher rates of obesity and metabolic disorders such as diabetes in people with IBD, that appear to be rising over the last decade, approaching 40%. Increased amounts of deep fat that surrounds abdominal organs such as the liver and intestines, known as visceral adipose tissue or VAT, is associated with more negative outcomes in those with IBD. Researchers have found evidence that VAT is a source of certain proteins called cytokines that trigger inflammatory responses by acting as chemical messengers. This is an important process in the presence of an injury or infection, but excessive amounts of these cytokines can lead to chronic inflammation and tissue damage, contributing to autoimmune diseases such as IBD, multiple sclerosis, and rheumatoid arthritis.
Is it possible to leverage the connection between obesity, metabolic disease, and IBD to improve IBD management? Recent studies have been exploring that very question, with promising results. The Journal of Crohn’s and Colitis published an article in October 2025 detailing the meta-analysis of 11 such studies, comprising a total of 16,242 patients with IBD and obesity and/or type 2 diabetes who received GLP-1 agonist treatment. The analysis compared the effects of GLP-1 agonist treatment with other treatments or placebos, and observed outcomes such as the need for corticosteroids, progression to advanced therapies like biologics, hospitalization, and surgery. The studies encompassed data from national registries in the United States, Denmark, and Israel, as well as from academic hospitals in the United States, Israel, and Spain.
Meta-analysis Findings
Across the 11 studies, patients treated with semaglutide, liraglutide, and tirzepatide achieved significant weight loss, particularly those with BMI > 30. Dulaglutide did not demonstrate statistically significant weight loss in this meta-analysis, and too few patients taking exenatide completed follow-up for it to be included in the findings. Patients taking GLP-1 agonists seemed to have similar rates of starting either corticosteroids or advanced therapies as those in the control group, with no real differences between those with ulcerative colitis vs. Crohn’s disease. When baseline BMI was considered, those with BMI < 30 had lower risk of corticosteroid initiation. This was possibly also the case for those with higher BMIs, though the numbers were too small to be conclusive.
Conversely, those with BMI > 30 who were treated with a GLP-1 agonist had lower risk of hospitalization. Data for those with lower BMI was suggestive of lower hospitalization risk but not conclusive. Patients with IBD who were treated with a GLP-1 agonist had significantly fewer surgical events overall. When factoring in BMI, those with BMI > 30 on GLP-1 agonist therapy had a lower risk of surgery, while treatment with a GLP-1 agonist did not seem to significantly impact the risk of surgery for those with lower BMIs.
Conclusion
In summary, the reviewers concluded that treatment with GLP-1 agonists significantly reduces weight and the risk of hospitalization and surgery in patients with IBD, while recognizing the limitations involved in retrospective review of multiple studies. Stratification by BMI and VAT should be more closely studied in future research to understand their impacts on clinical outcomes, but it seems clear that addressing obesity as an important underlying factor in IBD could be a game-changer.
References
Assessed and Endorsed by the MedReport Medical Review Board