Could Weight-Loss Injections Such as Ozempic and Mounjaro Also Prevent Cancer?

Obesity and Cancer: A Connection That Cannot Be Ignored

A comprehensive assessment published by the International Agency for Research on Cancer (IARC) in 2016 established that excess body fat has a causal relationship with at least 13 different types of adult cancer . Obesity-related cancers include colorectal cancer, liver cancer, pancreatic cancer, renal cell carcinoma, gallbladder cancer, gastric cardia cancer, thyroid cancer, postmenopausal breast cancer, endometrial cancer, ovarian cancer, meningioma, and multiple myeloma.

The biological basis of this connection is explained through several mechanisms. Obesity increases levels of insulin and leptin, which support tumor cell proliferation. In addition, obesity-related chronic inflammation and suppression of the antitumor immune response can facilitate carcinogenesis. Bariatric surgery studies have shown that sustained weight loss of 20–30% over 10 years significantly reduces the risk of obesity-related cancer. The problem is that bariatric surgery is applicable only in cases of severe obesity and is not a feasible cancer prevention strategy at the population level.

Incretin-Mimetic Drugs: A Class That Goes Beyond Weight Management

Glucagon-like peptide-1 receptor agonists (GLP-1RA — glucagon-like peptide-1 receptor agonists) work by mimicking GLP-1, a gut hormone discovered in the 1980s that regulates insulin secretion. When exenatide, the first GLP-1RA, was approved for type 2 diabetes in 2005, the powerful effects of these drugs on obesity had not yet been discovered. Two decades of clinical experience have revealed that these drugs have much broader systemic effects than expected.

Why do these figures matter? The 19% weight loss achieved with dual agonists such as tirzepatide comes quite close to the 20–30% threshold achieved with bariatric surgery. Since bariatric surgery has been shown to reduce the risk of obesity-related cancer, whether this degree of pharmacological weight loss could provide a similar protective effect is a natural hypothesis.

Do People Taking GLP-1 Drugs Develop Cancer Less Often? Epidemiological Findings

Pharmacoepidemiological studies seeking to answer this question have surged over the past two years. The number of publications retrieved by a PubMed search for «GLP-1 agonists and cancer» rose from 207 in 2023 to 361 in 2025. The review summarizes six large studies with different designs and geographical settings.

Some of these studies suggest that GLP-1RA use reduces the risk of obesity-related cancer by 30–60% . If this picture were indeed accurate, it would be striking, because this figure exceeds even the 20% reduction in cardiovascular events observed in patients with obesity taking semaglutide in the SELECT trial. However, the researchers emphasize that these data should be approached with caution.

In contrast, the Gamborg study in Denmark reported that GLP-1RA use slightly increased cancer risk. The researchers offered an interesting interpretation of this paradox: because of the survival advantage provided by GLP-1RAs, patients may live longer and reach a stage at which they are more likely to develop cancer. Analyses that do not account for this «competing risk» phenomenon appear capable of producing incorrect conclusions.

Why Are These Data Insufficient? Six Methodological Weaknesses

One of the most valuable sections of the review systematically identifies the methodological weaknesses in existing observational studies. These errors can make an association appear much stronger or much weaker than it really is.

It should also be noted that the vast majority of these studies were conducted in patient populations with type 2 diabetes and had average follow-up periods of 2–5 years. Considering that even interventions proven to reduce cancer risk, such as bariatric surgery, have shown significant effects at 10 years of follow-up, the value of data from studies with short follow-up periods is open to question.

How Might GLP-1 Drugs Prevent Cancer? Four Possible Pathways

Current data suggest four mechanisms through which incretin-mimetic drugs might reduce cancer risk; these mechanisms are not mutually exclusive. They may all operate together, and their relative importance has not yet been established.

Among these mechanisms, effects on the immune system are particularly noteworthy. Recent studies have shown that obesity suppresses CD8+ T-lymphocyte infiltration and that elevated leptin levels in obesity lead to T-cell dysfunction through PD-1. In endometrial cancer models, weight loss has been shown to reverse this T-cell suppression and lead to tumor regression. The weight loss produced by GLP-1RAs and their possible direct immunomodulatory effects may contribute to this mechanism.

There is also another mechanism specific to hepatocellular carcinoma: GLP-1RAs are known to improve fatty liver disease (steatohepatitis), and metabolic dysfunction-associated steatohepatitis is an important risk factor for liver cancer.

Why Is Conducting a Clinical Trial So Difficult?

The data look compelling, and the biological mechanisms are plausible — so why is there no randomized controlled cancer prevention trial? The PADRAIC research project (Preliminary Analysis to Design Anti-obesity Interventions to Prevent Adult Cancers) systematically answered this question. The resulting list of obstacles appears extremely challenging.

Modeling studies show that a trial designed for the «general population» would require more than 50000 participants and would not be practical. As a more feasible approach, the review authors suggest focusing on subpopulations in which obesity (BMI ≥27–35) coexists with precancerous conditions such as Barrett esophagus, endometrial hyperplasia, colon polyps, or liver fibrosis. This approach both reduces the required sample size and makes it easier to obtain meaningful results within a shorter time frame.

Side Effects of GLP-1 Drugs: How Acceptable Are They in Cancer Prevention?

For a drug to be used for cancer prevention, its safety profile must be clinically acceptable when administered to healthy individuals. How should the existing GLP-1RA safety data be interpreted in this context?

The authors conclude that the available safety data would methodologically permit the use of GLP-1RAs for cancer prevention — but this assessment is conditional on the reduction in cancer risk being clinically meaningful.

This article was created using various editorial tools, including artificial intelligence, as part of the process. It was reviewed by human editors before publication.