Ozempic, Wegovy, Mounjaro and Zepbound are best known for blood sugar and weight. A wave of 2025–2026 research suggests they may also reduce the risk of tuberculosis and other serious infections.
Yes, according to a growing body of evidence — though "reduce infection rates" is a more accurate description than anything more dramatic. A large 2025 meta-analysis of 136 randomized trials found GLP-1 drugs were associated with an 11% lower relative risk of serious infections. Two new 2026 studies add to that picture: one linking GLP-1 use to significantly lower tuberculosis rates, and another linking tirzepatide to fewer infection-related hospitalizations and deaths. None of this is proven cause-and-effect yet, and none of it is an approved use — but the pattern is consistent enough that researchers are taking it seriously.
The most rigorous piece of evidence here comes from a systematic review and meta-analysis published in the Journal of Infection, pooling data from 136 randomized controlled trials and roughly 164,000 participants. Because it's built from randomized trials rather than just observational records, it's better positioned to support a real cause-and-effect relationship, not just a correlation.
The findings: GLP-1 receptor agonist treatment was associated with an 11% lower relative risk of serious infections requiring hospitalization or advanced care, along with smaller but still significant reductions in non-serious and total infections. Looking at specific body systems, the reduction showed up most clearly in serious respiratory infections, skin and soft tissue infections, musculoskeletal infections, and vascular infections. COVID-19 risk was also lower among GLP-1 users in the pooled trial data.
One particularly useful detail from this analysis: the benefit appears to scale with how much a person's metabolic health improved. Patients who lost more than 3 kg during their trial had a meaningfully lower infection risk than those who lost less weight, and among people with diabetes, larger A1C reductions were also tied to greater infection-risk reduction. That's a dose-response pattern — more metabolic improvement, more protection — which is one of the stronger signals researchers look for when trying to determine whether an association is causal.
Two more recent studies, both published within the past several weeks, add real-world weight to the trial data.
The first, published in Nature Communications in August 2026, looked specifically at tuberculosis — a bacterial infection that killed roughly 1.2 million people globally in 2024 and can lie dormant in the body for years before resurfacing when the immune system weakens. Using a large multicenter cohort of medical records, researchers compared people with type 2 diabetes taking a GLP-1 drug against those taking other common diabetes medications (DPP-4 inhibitors, sulfonylureas, metformin, and SGLT2 inhibitors) between 2017 and 2025. GLP-1 users had an 18–51% lower risk of developing active tuberculosis, a benefit that held for up to five years of follow-up.
The second, published in the BMJ in August 2026, was primarily a cardiovascular study — researchers were investigating how tirzepatide affected heart health in people with type 2 diabetes and existing cardiovascular disease, compared to an older diabetes drug. Tirzepatide reduced major cardiovascular events, as expected. But the researchers also noticed something else: tirzepatide users were less likely to be hospitalized for an infection, and less likely to die during the study period, including specifically from infection. The study authors floated the idea that part of the survival benefit they measured may not be purely cardiovascular — some of it may reflect this separate, less-expected reduction in serious bacterial infections.
Nobody has nailed down the exact mechanism yet, but there are a few plausible, non-exclusive explanations researchers are working through:
It's worth being precise about the limits of this evidence. Both the tuberculosis study and the tirzepatide-hospitalization study are observational and retrospective — they can show a correlation, not prove that the drug directly caused fewer infections. People who are prescribed and stay on GLP-1 drugs may differ from those who don't in ways that also affect infection risk (access to care, other health conditions, follow-up frequency), and even careful statistical adjustment can't fully rule that out.
The meta-analysis of randomized trials is stronger evidence because randomization limits that kind of bias, but even its authors are careful to note that further research, including prospective studies designed specifically to test this question, is needed before infection prevention becomes any kind of clinical recommendation. No GLP-1 drug is approved or indicated for preventing infections, and none of this evidence should be used to decide whether or not to start one.
The pattern showing up across multiple independent studies — a randomized-trial meta-analysis, a tuberculosis cohort study, and a cardiovascular trial with an unexpected side finding — is consistent enough that it's a genuinely active area of research, not a one-off statistical fluke. For people already taking Ozempic, Wegovy, Mounjaro, or Zepbound for diabetes or weight management, a reduced infection risk may be a welcome bonus layered on top of the drugs' established benefits. It's not, at this point, a reason on its own to start one. For more on how these drugs work and compare, see our full GLP-1 comparison, and for the surprising origin story of the drug class, see our history of GLP-1 drugs.