A new study has found that the keto diet, which relies on consuming large amounts of fat and reducing carbohydrates, may not have the same effect on cancer as previously thought.
The study showed that its effect varies depending on the affected part of the intestine; it may help reduce tumor growth in the colon, but it may stimulate their growth in the small intestine.
The ketogenic diet is one of the most popular diets in the world. It was first used decades ago to help control epilepsy, and research has since expanded to include weight loss and various diseases, including Alzheimer's and cancer. However, researchers are still trying to understand how this diet affects different organs in the body.
A team of researchers at the Massachusetts Institute of Technology studied the effect of the ketogenic diet on genetically modified mice that developed tumors in the intestines, with the aim of finding out if the benefits identified by previous research in colon cancer extend to the rest of the digestive system.
The researchers subjected the mice to three different diets: a high-fat, low-carbohydrate keto diet, a normal diet for comparison, and a high-fat, high-calorie diet commonly used to induce obesity.
The results showed that the keto diet led to contradictory results; it was associated with increased tumor growth in the small intestine, while it continued to reduce tumor growth in the colon, which is consistent with the results of previous studies.
Surprisingly, the cause was not ketone bodies, which are molecules produced by the body when relying on fat as a primary source of energy, as some researchers had believed, but rather the way intestinal cells deal with the fats the body obtains from food.
The researchers explained that when intestinal cells break down fats to obtain energy, they activate proteins known as "PPAR," and these proteins stimulate intestinal stem cells to divide at a faster rate.
Stem cells in the intestines play an important role in tissue regeneration and damage repair, but increased activity can also carry a risk, as it raises the likelihood of changes that lead to tumor formation.
Omar Yilmaz, a biologist and pathologist at MIT and the study's lead author, said that increasing the number of stem cells helps the small intestine repair itself better, but it may also make these cells more prone to turning into cancerous cells.
As Jessica Shay, a researcher involved in the study, explained, diet and metabolism are not necessarily the same thing, noting that the study's results underscore the importance of distinguishing between the effect of the keto diet itself and the effect of ketone supplements.
She added that researchers initially expected that ketone bodies, especially the compound beta-hydroxybutyrate (BHB), would be the direct factor behind the effects of the keto diet on cancer, but the results showed that they only play a secondary role.
The team emphasized that the results do not necessarily mean the keto diet causes cancer in humans, as the experiments were conducted on an animal model genetically engineered to develop intestinal tumors. This model resembles familial adenomatous polyposis in humans, a rare genetic condition that increases the risk of developing intestinal tumors.
The researchers noted the need for further studies to determine whether the same mechanisms occur in humans. They also explained that commercially available ketone supplements may not produce the same effects, as the results were related to the way fats are metabolized within cells and not simply to raising ketone levels in the body.
The team is currently working to understand why the small intestine and colon respond differently to the same diet, in an effort to understand the complex relationship between nutrition and tumor growth.
The study was published in the journal Nature.
