The keto diet is not as safe as it seems: an experiment has revealed hidden risks

A study at the University of Utah Health medical center showed that long-term adherence to the ketogenic diet in mice gradually leads to metabolic damage. This was reported by writes Earth.com.

For over nine months, the animals were on a special diet, after which their bodies were subjected to a "carbohydrate challenge." By tracking blood fat levels and sugar response, researchers discovered metabolic problems that had gone unnoticed for months when only weight was assessed.

Almost completely eliminating carbohydrates forced the mice to use fat as their primary energy source. This metabolic state, known as ketosis, where the body replaces glucose with ketones, can lower blood sugar levels in the short term.

Over the course of several months, mice on the ketogenic diet gained significantly less weight than those on a high-fat "Western" diet. However, most of the weight they did gain was fat tissue rather than muscle, which altered their body composition.

The traditional ketogenic diet in this experiment provided about 90% of calories from fat, with almost no carbohydrates. Such an extreme balance limited weight gain but at the same time increased the risk of problems with blood biochemistry.

Although the mice appeared thin, their blood showed an excess of fats, a condition known as hyperlipidemia. Elevated triglycerides, the main form of fat in the blood, appeared in the early stages and remained high throughout the feeding period. This created an additional burden on the body, so blood parameters were significant even before changes in weight.

In male mice, fat accumulated in the liver, leading to the development of fatty liver disease. The abnormalities manifested when the liver lost its ability to function normally, affecting fat processing. Female mice on a ketogenic diet were mostly protected from such deposits, and this sex difference remained unexplained.

After two to three months on a ketogenic diet, mice showed decreased blood sugar and insulin levels, which initially seemed positive. However, even a small amount of carbohydrates caused glucose intolerance: blood sugar levels remained elevated for too long due to insufficient insulin secretion by the pancreas. This prolonged increase in glucose indicated impaired pancreatic function, which usually responds quickly by producing insulin.

Researchers found that the mice remained sensitive to insulin, but did not secrete enough of it after glucose was introduced.

Insulin is a hormone that transports sugar into cells and is usually produced by the pancreas within a few minutes.

In mice on a ketogenic diet, the beta cells responsible for its synthesis showed signs of stress in areas related to protein processing. Electron images showed swelling of the Golgi apparatus, a structure that packages proteins. This presumably slowed down insulin secretion.

Stopping the diet had an unexpected benefit: four weeks of low-fat eating restored normal glucose processing in the males. The rapid recovery indicated that the pancreas is capable of rebuilding the insulin release system once the influence of excess fat is reduced.

After returning to a "Western" diet, the weight loss was not maintained, which showed that keto does not prevent further weight regain.