Scientists discovered that obesity changes how the body produces certain fat-like molecules in the colon that normally protect against cancer. Using advanced lab techniques, researchers found that obese mice with colon cancer had much lower levels of protective molecules called fatty acid epoxides, while having higher levels of cancer-promoting molecules. The genes that make the protective molecules were also turned down by 70-96%, while genes that break down these protective molecules were turned up. This discovery suggests that obesity disrupts a specific chemical pathway in the body, which may explain why overweight people have a higher risk of developing colon cancer.

The Quick Take

  • What they studied: How obesity changes the levels of special fat-like signaling molecules in the colon that may protect against or promote cancer development
  • Who participated: Laboratory mice—some that were obese with colon cancer and some that were lean and healthy—used to model how obesity affects cancer risk in humans
  • Key finding: Obese mice with colon cancer had 40-76% less of a protective molecule called fatty acid epoxides compared to healthy lean mice, while also having increased levels of cancer-promoting molecules
  • What it means for you: This research suggests that obesity may increase colon cancer risk by disrupting the body’s natural protective chemical systems. While this is early-stage research in mice, it could eventually lead to new ways to prevent or treat obesity-related colon cancer in humans. Talk to your doctor about colon cancer screening if you’re overweight or have family history of cancer.

The Research Details

Researchers used mice to study how obesity and colon cancer affect special fat-like molecules called eicosanoids. They created two groups: obese mice fed a high-fat diet that developed colon cancer, and lean healthy mice as controls. The scientists used a sophisticated lab technique called LC-MS/MS (a type of chemical analysis) to measure over 100 different eicosanoid molecules in the colons of both groups. They also examined which genes were turned on or off in the colon tissue to understand why the eicosanoid levels changed.

This approach allowed researchers to get a detailed picture of how obesity changes the chemical environment in the colon. The high-fat diet model mimics how obesity develops in humans, making the findings potentially relevant to human health. By measuring so many different molecules at once, the scientists could see patterns that might have been missed by looking at just one or two molecules.

Understanding the specific chemical changes that happen in obesity-related colon cancer is important because it could lead to new prevention and treatment strategies. Previous research focused mainly on one pathway (the COX pathway), but this study reveals that another pathway (the CYP pathway) may be equally or more important. By identifying which molecules are reduced and which genes are affected, scientists can develop targeted treatments that restore the protective molecules or block the harmful ones.

This study was published in a respected nutrition science journal and used advanced, precise laboratory techniques to measure eicosanoids. The findings were supported by both chemical measurements and gene expression analysis, which strengthens confidence in the results. However, this is animal research in mice, which doesn’t always translate directly to humans. The study provides important clues but would need to be confirmed in human studies before changing medical practice.

What the Results Show

The most striking finding was that obese mice with colon cancer had dramatically lower levels of protective fatty acid epoxides—between 40-76% lower than lean healthy mice. At the same time, these obese mice had higher levels of cancer-promoting molecules like prostaglandin E2. The researchers also found that the genes responsible for making the protective epoxides were severely reduced, with some genes turned down by 70-96%. Conversely, the gene that breaks down these protective molecules (called soluble epoxide hydrolase) was increased by about 43% in obese mice with cancer.

This pattern suggests that obesity creates a double problem: the body makes less of the protective molecules while simultaneously making more of the molecules that break them down. This combination could explain why obese individuals have higher colon cancer risk.

The study confirmed that established cancer-promoting molecules (like COX-derived prostaglandins) were indeed increased in obese mice with cancer, which aligns with previous research. However, the surprising discovery was that the CYP pathway changes were even more dramatic than the COX pathway changes, suggesting this pathway may play a larger role in obesity-related colon cancer than previously thought. The gene expression patterns perfectly matched the chemical measurements, indicating that the reduced protective molecules were due to reduced production rather than other factors.

Previous research had focused mainly on the COX pathway in obesity-related colon cancer, and this study confirms those findings. However, this research reveals that the CYP pathway may be equally or more important than previously recognized. While the COX pathway has been studied in clinical trials, the CYP pathway has received less attention. This study suggests that future research and treatments should focus more on restoring the protective fatty acid epoxides that are reduced in obesity-related colon cancer.

This study was conducted in mice, not humans, so the findings may not directly apply to people. The researchers didn’t test whether restoring the protective molecules would actually prevent cancer, only that the molecules were reduced. The study doesn’t explain exactly why obesity causes these chemical changes, only that it does. Additionally, the sample size of mice wasn’t specified in the abstract, making it difficult to assess statistical power. Human studies would be needed to confirm whether these findings apply to colon cancer risk in overweight and obese people.

The Bottom Line

Based on this research, the strongest evidence-based recommendation remains maintaining a healthy weight through balanced diet and regular physical activity, as obesity is a known risk factor for colon cancer. This study suggests that the protective mechanisms disrupted by obesity involve multiple chemical pathways, supporting the importance of weight management. Standard colon cancer screening recommendations should be followed, especially for people who are overweight or obese. While this research is promising, it’s too early to recommend specific supplements or treatments targeting the CYP pathway—more research is needed.

This research is most relevant to people who are overweight or obese, particularly those with family history of colon cancer. Healthcare providers and researchers studying obesity and cancer should pay attention to these findings. People already following healthy lifestyle recommendations don’t need to change their approach based on this single study. Those with existing colon cancer or precancerous polyps should discuss this research with their oncologist, though it doesn’t change current treatment approaches.

This is early-stage research, so practical applications are likely years away. If this research leads to new treatments, it would typically take 5-10 years of additional human studies before becoming available. In the meantime, the most immediate benefit is understanding that obesity affects cancer risk through multiple chemical pathways, reinforcing the importance of weight management now rather than waiting for future treatments.

Want to Apply This Research?

  • Track weekly weight and waist circumference measurements alongside dietary fat intake (grams per day) to monitor progress toward a healthier weight. This creates a personal connection between diet choices and body composition changes that relate to cancer risk factors.
  • Set a goal to reduce high-fat food intake by replacing one high-fat meal per week with a lower-fat option, while increasing fiber intake from vegetables and whole grains. Use the app to log these swaps and track how they affect weight over 8-12 weeks.
  • Create a monthly dashboard showing weight trends, dietary fat intake patterns, and physical activity levels. Set reminders for annual colon cancer screening appointments (starting at age 45 or earlier if family history exists) and track completion in the app. Monitor for any digestive changes and log them to discuss with healthcare providers.

This research was conducted in mice and has not been tested in humans. The findings are preliminary and do not yet change medical recommendations for colon cancer prevention or treatment. This article is for educational purposes only and should not replace professional medical advice. If you have concerns about colon cancer risk, obesity, or any health condition, please consult with your healthcare provider. Do not start, stop, or change any medications or supplements based on this research without talking to your doctor first. Current colon cancer screening guidelines should be followed regardless of this research.