A new study suggests that high levels of dietary fructose can cause liver damage even without any association with weight gain, according to an animal study.
Earlier this week the Digital Journal reported that too much sugar in a diet appears to be a trigger for heart problems, according to new research. Certain types of glucose appear to have an adverse effect on heart muscle. Now comes a new study looking at a certain type of sugar - fructose - and the effect on the liver.
In the study, scientists compared two groups of animals. One group was fed a high-fructose diet (where about a quarter if the foods consumed contained fructose) and the other group was fed a standard feed diet. The study was conducted on monkeys. None of the monkeys in the study had ever previously consumed fructose.
Fructose, or fruit sugar, is a simple monosaccharide found in many plants, which is also similar to sucrose. Medics have been concerned for a few years that excessive fructose consumption may contribute to the development of non-alcoholic fatty liver disease.
Both diets had the same amount of fat, carbohydrate and protein, but the sources were different: the high-fructose group's diet was made from flour, butter, pork fat, eggs and fructose (the main ingredient in corn syrup), similar to what many people eat, while the control group's diet was made from healthy complex carbohydrates and soy protein.
The researchers found that over a six-week study period liver damage more than doubled in the animals fed a high-fructose diet as compared to those in the control group. The researchers measured biomarkers of liver damage through blood samples to assess the extent of the damage.
Putting aside the ethics of testing monkeys with a ‘western’ sugary diet, the findings do indicate that the high availability of certain convenience foods is of concern if such foods are consumed in high quantities.
The findings have been published in the journal American Journal of Clinical Nutrition. The paper is titled “Dietary fructose induces endotoxemia and hepatic injury in calorically controlled primates.”