For years, ketogenic diets have been promoted as a powerful way to lose weight, improve blood sugar levels, and even support healthy aging.
Scientists have also investigated whether these high-fat, low-carbohydrate diets might help fight cancer. A new study from MIT suggests the answer is more complicated than many people expected. According to research published in Nature, the same diet that appears to protect against colon cancer may actually encourage tumors to grow in another part of the digestive system.
A ketogenic diet changes the body’s normal source of energy. Instead of relying mainly on carbohydrates, the body burns fat and produces ketone bodies.
These ketones have attracted enormous scientific interest because they can fuel the brain during fasting and have been linked to several possible health benefits. Some previous studies even suggested that ketones themselves could slow the growth of colon cancer.
The MIT researchers wanted to see whether the same protection occurred in the small intestine. They used mice that were genetically likely to develop intestinal tumors and compared animals eating a ketogenic diet with mice eating either a regular diet or a high-calorie, high-fat diet.
The results were unexpected. Mice on the ketogenic diet developed many more tumors in the small intestine than mice eating a normal diet. Their cancer risk was similar to, and sometimes even greater than, that of mice eating the calorie-rich diet, despite the ketogenic mice remaining relatively lean.
Further experiments revealed why this happened. Rather than ketones causing the problem, the researchers found that intestinal stem cells were responding to the large amount of dietary fat.
As these cells burned more fat for energy, a biological pathway involving proteins called PPARs became highly active. This stimulated the stem cells to multiply rapidly. Although extra stem cells help repair damaged intestinal tissue, excessive growth also increases the chance that some cells will become cancerous.
In contrast, the colon responded very differently. The ketogenic diet reduced tumor formation there, confirming earlier studies. Surprisingly, ketones were not responsible for this protection either. Both the harmful effects in the small intestine and the beneficial effects in the colon were linked mainly to how each tissue handled dietary fat.
The findings may also reassure people who occasionally consume ketone supplements. Because the observed effects were driven by fat metabolism rather than ketones themselves, the researchers do not expect ketone drinks alone to produce either the benefits or the risks seen in this study.
The scientists now want to understand why two neighboring organs react so differently to exactly the same diet. Solving this mystery may improve understanding of cancer biology and help doctors provide more personalized nutrition advice in the future.
This research has important limitations. The experiments were conducted in genetically engineered mice, not in human volunteers.
Human digestive systems and eating patterns are more complex, so additional studies will be required before dietary recommendations change. Even so, the work highlights that popular diets should be studied carefully instead of assuming they have the same effects throughout the body.
Overall, this study provides valuable new insights into how diet influences cancer risk. It demonstrates that the relationship between nutrition and cancer is highly tissue-specific, and it reminds us that no single diet is likely to be ideal for every person or every organ.
Future human research will determine whether these findings should influence dietary advice for people at high risk of intestinal cancer.
If you care about cancer, please read studies that artificial sweeteners are linked to higher cancer risk, and how drinking milk affects risks of heart disease and cancer.
For more health information, please see recent studies about the best time to take vitamins to prevent heart disease, and results showing vitamin D supplements strongly reduces cancer death.
Source: Massachusetts Institute of Technology (MIT).
