Researchers discovered that two compounds made by gut bacteria—called TMA and TMAO—may help colon cancer cells grow faster and spread more easily. In lab experiments and mice, these substances activated a specific protein that made cancer cells multiply and resist death. The study suggests that reducing these compounds through diet or using special drugs to block the protein might slow down colon cancer. This finding could lead to new ways to prevent or treat colorectal cancer, one of the most common cancers worldwide.

The Quick Take

  • What they studied: Whether two gut bacteria byproducts (TMA and TMAO) help colon cancer cells grow and what biological switches they flip to do this
  • Who participated: Lab-grown colon cancer cells and laboratory mice with implanted human colon cancer tumors
  • Key finding: Both TMA and TMAO made colon cancer cells multiply faster, move more easily to other places, and resist dying. Mice fed a high-TMAO diet developed larger tumors than control mice.
  • What it means for you: If you have risk factors for colon cancer, reducing foods that create these compounds (like red meat and eggs) might help. However, this is early research in lab settings—talk to your doctor before making major dietary changes based on this study alone.

The Research Details

Scientists used multiple approaches to understand how TMA and TMAO affect colon cancer. First, they grew human colon cancer cells in dishes and exposed them to different amounts of TMA and TMAO, then measured how the cells responded. They used several techniques to see which genes and proteins changed. They also examined individual cells using advanced sequencing technology to understand exactly what was happening inside them. Finally, they implanted human colon cancer cells into mice and fed some mice a diet high in TMAO to see if it affected tumor growth in living animals.

The researchers measured cell growth, cell movement, whether cells died naturally, and changes in specific proteins. They looked particularly at a protein called SREBF1 and a cellular pathway called PI3K/AKT that helps cells survive and multiply.

This combination of lab experiments and animal studies allowed the researchers to move from understanding what happens in a dish to seeing if it matters in a living organism.

This research approach is important because it bridges the gap between what we observe in nature and what actually causes disease. By studying both cells and whole animals, researchers can be more confident that their findings might apply to humans. The use of advanced genetic sequencing helps identify exactly which cellular processes are affected, which could lead to better drug targets.

The study used established scientific methods and multiple complementary approaches, which strengthens confidence in the findings. However, the research was conducted in laboratory settings and mice, not humans, so results may not directly translate to people. The specific doses used in lab experiments may not match what people experience from food. The journal publishes environmental and toxicology research, which is appropriate for this topic. The study would benefit from human clinical data to confirm these mechanisms actually occur in colon cancer patients.

What the Results Show

When colon cancer cells were exposed to TMA and TMAO in the lab, the cells multiplied significantly faster than untreated cells. The most dramatic effects occurred at specific doses: 1 microgram of TMA and 100 micrograms of TMAO per milliliter. At these doses, cancer cells not only grew faster but also became better at invading surrounding tissue and migrating to other locations—key features of aggressive cancer.

The researchers discovered that TMA and TMAO worked by activating a protein called SREBF1 and turning on a cellular pathway called PI3K/AKT. Think of these like switches that tell cancer cells to grow and survive. When these switches were activated, cancer cells resisted natural cell death (apoptosis), which normally stops damaged cells from becoming cancerous.

In mice, the effect was clear: animals fed a high-TMAO diet developed significantly larger tumors than mice on a normal diet. This suggests that dietary TMAO levels can influence cancer growth in living organisms, not just in lab dishes.

The single-cell analysis revealed that different cancer cells responded somewhat differently to TMA and TMAO exposure, suggesting that not all cancer cells are equally affected. This could explain why some people might be more vulnerable to these compounds than others. The study also showed that the effects were dose-dependent—meaning higher amounts of these compounds had stronger effects on cancer cell behavior.

Previous research had linked high TMAO levels to various diseases including heart disease and kidney disease, but the specific mechanisms in colon cancer were unclear. This study provides the first detailed explanation of how TMA and TMAO specifically promote colon cancer cell growth through the SREBF1 and PI3K/AKT pathways. The findings align with growing evidence that gut bacteria composition influences cancer risk, though most prior work focused on bacterial species rather than their metabolic byproducts.

This research was conducted entirely in laboratory settings and mice, not in humans, so we cannot yet confirm these mechanisms occur in actual colon cancer patients. The doses used in experiments may not reflect what people consume through food. The study doesn’t explain individual differences in how people produce or respond to these compounds. Additionally, the research doesn’t account for other dietary factors or lifestyle elements that influence colon cancer risk. Finally, while the study suggests SREBF1 inhibitors might help, no such drugs have been tested in humans for this purpose yet.

The Bottom Line

Based on this research (moderate confidence level): Consider reducing consumption of foods that produce high levels of TMA and TMAO, particularly red meat, processed meat, and high-fat dairy products. These foods contain precursors that gut bacteria convert into TMA and TMAO. Increasing fiber intake through vegetables, fruits, and whole grains may help maintain healthier gut bacteria that produce fewer of these compounds. However, these recommendations should complement, not replace, standard colon cancer screening and prevention guidelines recommended by your doctor.

This research is most relevant for people with a family history of colon cancer, those over 45 (standard screening age), and people with inflammatory bowel disease. It’s also important for anyone interested in cancer prevention through diet. This research should NOT be used as a substitute for medical advice or standard cancer screening. People already diagnosed with colon cancer should discuss dietary changes with their oncology team.

Changes in gut bacteria composition typically take 2-4 weeks to show up after dietary changes. However, any impact on actual cancer risk or progression would take much longer to observe—likely months to years. This is early-stage research, so don’t expect immediate health changes from dietary adjustments based on this study alone.

Want to Apply This Research?

  • Track weekly consumption of red meat, processed meat, and high-fat dairy products (in servings per week) alongside daily fiber intake (in grams). Monitor these trends over 8-12 weeks to see if you’re successfully reducing TMAO-producing foods while increasing fiber.
  • Set a specific goal like ‘Replace 2 red meat meals per week with plant-based proteins’ or ‘Add one extra vegetable serving daily.’ Use the app to log these substitutions and track consistency. Create reminders for high-fiber snacks like berries, nuts, or whole grain crackers.
  • Establish a baseline of current eating patterns, then track changes monthly. Set quarterly check-ins to assess whether dietary modifications feel sustainable. If available, discuss with your doctor about periodic TMAO blood testing to see if your levels are decreasing with dietary changes.

This research describes laboratory and animal studies, not human clinical trials. The findings suggest potential mechanisms but do not prove that dietary changes will prevent or treat colon cancer in people. This information is educational and should not replace professional medical advice, diagnosis, or treatment. If you have concerns about colon cancer risk or are experiencing symptoms, consult with a qualified healthcare provider. Anyone with a personal or family history of colorectal cancer should follow screening guidelines recommended by their physician, regardless of dietary modifications. Do not stop or change cancer treatments based on this research without explicit guidance from your oncology team.