Wednesday, July 29th 2026
New study in mice found completely opposite effects on the small and large intestine, while scientists suspect that the key is not ketones, but the way cells process fat
The ketogenic diet has been among the most popular nutrition regimes for years. Some use it for weight loss, others for diabetes control, while in recent years scientists are also investigating its possible influence on the development of certain types of cancer.
However, a new study published in the prestigious journal Nature shows that the answer is not simple at all. The researchers found that the same diet can have opposite effects in different parts of the intestine: in the large intestine it slowed the development of tumors, while in the small intestine it promoted their growth in mice with a genetic predisposition.
Even more surprising was the fact that the cause did not seem to be ketones, as previously thought, but the way the cells of the intestine process and burn fats.
Scientists expected a result, but found the opposite
Researchers from the Massachusetts Institute of Technology, MIT, wanted to check whether the protective effect of the keto diet, previously observed in colon cancer, could also appear in other parts of the digestive system.
The experiment used genetically modified mice, which had a tendency to develop intestinal tumors. They were divided into three groups: one group followed a ketogenic diet, one group a control diet and the third group a diet very rich in fat and calories, commonly used as a model for obesity.
The results surprised even the researchers themselves.
Mice following this diet developed more tumors in the small intestine and had shorter survival than those fed the usual diet. Although they did not become obese, the rate of tumor development was similar or even higher than in mice fed an obesogenic diet.
At the same time, in the large intestine, the keto diet showed the opposite effect and inhibited the formation of tumors, Telegrafi reports.
The problem may not be ketones, but fat burning
Until now, it was thought that the possible protective effects of the keto diet were mainly related to the bodies ketones, especially with beta-hydroxybutyrate, BHB.
This molecule is created when the body, due to a lack of carbohydrates, begins to use fats as its main source of energy.
A 2022 study had suggested that BHB could decrease the proliferation of cells in the colon and inhibit the growth of colorectal tumors.
But the new study shows that ketones may not be the factors main.
Researchers genetically altered the processes of production and use of ketones, but this did not change the development of tumors. According to them, the main role was played by the oxidation of fatty acids, that is, the way the cells of the small intestine burn fats for energy.
During the metabolism of fats, a family of proteins called PPARs is activated. These signal the intestinal stem cells to multiply faster.
On the one hand, the greater number of stem cells helps to regenerate the intestinal mucosa more quickly after disease or injury.
On the other hand, the more often the cells divide, the greater the probability that some of them may undergo changes that contribute to the formation of tumors.
So, the same mechanism that helps tissue repair, under certain circumstances it may even favor the development of cancer.
New study challenges an important theory
The results are particularly interesting because they call into question the idea that ketones are responsible for the effects of the keto diet on intestinal tumors.
The authors of the study described ketones as almost “metabolic bystanders”, while the main effects were related to the processing of large amounts of fat by cells source.
For this reason, commercial ketone supplements or drinks are not necessarily expected to produce the same effects as the ketogenic diet. An increase in the level of ketones in the blood does not mean that the same metabolic processes develop in the body as during a long-term high-fat, very low-carbohydrate diet.
The most important limitation of the study is that it was conducted in mice with a genetic predisposition to intestinal tumors.
In humans, this can best be compared to familial adenomatous polyposis, a rare inherited disease that significantly increases the risk of intestinal tumors.
Therefore, the results cannot be directly applied to humans and do not prove that these diets cause cancer.
Clinical studies are needed to determine whether similar mechanisms occur in humans, as well as to understand why the small intestine and large intestine respond so differently to the same diet.
The main message of the study is that the effects of diets can vary not only from person to person, but also from one intestinal tissue to another. the other. A regimen that may have a protective effect in one part of the organism may be unfavorable in another.
Source: prizrenpost
