A lot of fat, few carbohydrates: these are the principles of a ketogenic diet from which some help hope to lose weight. But how does this diet affect health in the long term? Researchers have now examined this on mice. The ketogenic animals initially lost weight, but developed health problems such as fatty liver, glucose intolerance and a greatly increased cholesterol level within a year. From the researchers’ point of view, the results indicate that long -term ketogenic diet of health harms rather than benefits.
A ketogenic diet is supposed to put the body into a state of ketosis in which it prefers its energy from fat instead of carbohydrates – and thus reduces stubborn fat pads. While the German Society for Food Healthy Adults recommends at least half of their energy requirements to cover with carbohydrates, around 90 percent of the calories are said to come from fat in a ketogenic diet. The diet in people with epilepsy can help reduce seizures. In some cases, however, ketogenic diets are also recommended for losing weight or against diabetes. “However, their long -term effects on metabolic health have not yet been sufficiently researched,” warns a team around Molly Gallop from the University of Utah in Salt Lake City.
Fluctuating weight
Gallop and her colleagues have tested on mice, which causes a permanent ketogenic diet in the body. To do this, they divided the animals into several groups: a group fed them for almost a year according to the specifications of a ketogenic diet with plenty of fat and little carbohydrates (KD). Regular blood analyzes confirmed that these animals were actually consistently in the state of ketosis. Another group received a diet in which 60 percent of the calories come from fat and which is usually used to generate obese mice (HfD). Two other groups were fed with only ten percent of the calories made of fat (LFD). In all cases, it was left to the mice how much they consumed from the respective feed.
It showed that while the mice with the 60 percent fat diet increased quickly, the keto mice could keep their weight or even reduce slightly in the first few weeks-similar to the fat-low mice. The extent to which this was actually due to ketosis is unclear: “These differences can at least partially be explained by the fact that the keto mice ate out of fewer than their fellow species with the 60 percent fat diet,” explains the research team.
After around ten weeks, however, the keto mice began to add weight. In the following months they did not get as thick as the 60 percent fat mice, but they achieved a similar body fat share. “The ketogenic diet did not lead to a reduction in body weight in the long term and should therefore not be regarded as a measure against overweight or diabetes,” write Gallop and her team.
Metabolism from balance
In addition, the researchers found increasing metabolic problems in the keto mice: “The longer the animals were fed ketogenic, the more they developed a glucose intolerance and disturbed insulin secretion,” reports the team. In contrast to the 60 percent fat mice, which with increasing weight developed a resistance to insulin, as it is typical of diabetes, the keto mice became more sensitive to insulin. However, their island cells in the pancreas, which are usually responsible for insulin release, were damaged by the ketogenic diet so that they hardly produced insulin. In addition, the keto mice showed greatly increased cholesterol levels, which are associated with cardiovascular diseases in humans. In addition, the animals developed fatty liver within a few months.
The knowledge gained from mice is not directly transferable to humans, but report with reports that patients who feed ketogenic in the long term due to epilepsy suffer more often from cardiovascular diseases, high blood lipid levels and pancreatitis. “Taken together, these results indicate that long -term ketogenic diet leads to a variety of negative changes in metabolic parameters that question systematic use as health -promoting nutritional intervention,” conclude the researchers.
Source: Molly Gallop (University of Utah) et al., Science Advances, Doi: 10.1126/sciadv.adx2752