A study on mice suggests the Keto diet may carry a small intestinal cancer risk for those predisposed to the disease

The ketogenic diet may heighten the likelihood of developing small intestinal cancer in individuals with a genetic susceptibility to the disease, new research has revealed.

The findings, published in the prestigious journal Nature, demonstrated that mice predisposed to intestinal malignancies grew more tumours when fed a high-fat, low-carbohydrate ketogenic regimen compared to those on standard diets.

This discovery stands in stark contrast to earlier studies, which had indicated that keto eating plans might offer protective benefits against colon cancer.

It also raises significant questions about how this widely adopted dietary approach affects various regions of the digestive tract differently.

Scientists from the Massachusetts Institute of Technology identified the precise biological mechanism driving this increased cancer risk.

Dietary fats consumed as part of the ketogenic regimen triggered a cellular signalling pathway called PPAR-delta, rather than the ketone bodies produced during ketosis.

This activation substantially boosted the function of intestinal stem cells, which ordinarily serve to continuously regenerate the gut lining.

However, when these stem cells harbour genetic mutations, they can become the origin point for tumour development.

The research team explained that dietary interventions can produce markedly different outcomes across various bodily tissues, underscoring the complexity of nutritional impacts on health.

The ketogenic diet has surged in popularity across the Atlantic, with an International Food Information Council survey revealing that seven per cent of American adults were adhering to the regimen in 2022.

Originally devised as a treatment for epilepsy, the eating plan has since gained widespread adoption for weight management and blood sugar regulation.

The diet functions by severely limiting carbohydrate consumption to 50 grams daily or fewer, compelling the body to utilise fat rather than glucose for energy.

This metabolic shift induces a state known as ketosis, wherein ketone bodies accumulate in the bloodstream, giving the diet its distinctive name.

The researchers stressed that these observations were made in mice genetically prone to intestinal cancer, not in healthy human subjects.

Further investigation is required to establish whether identical mechanisms operate in people and which populations might face elevated vulnerability.

The study contributes to an expanding body of evidence demonstrating that the interplay between dietary choices and cancer development is far from straightforward.

Although ketogenic diets have been explored as therapies for certain conditions and may deliver metabolic advantages for some individuals, the findings suggest their effects are not universally advantageous.

Future research will examine how particular dietary fats influence cancer risk.