Dietary fructose linked to liver damage by gut bacteria mechanism: Animal data

By Nathan Gray contact

- Last updated on GMT

Related tags: Fatty liver

Dietary fructose linked to liver damage by gut bacteria mechanism
A high intake of dietary fructose may lead to ‘rapid’ liver damage from bacteria even in those who do not gain weight, according to new data in monkeys.

The new animal data, published in theAmerican Journal of Clinical Nutrition, ​suggests that intake of fructose may lead to rapid and significant liver damage irrespective of calories or weight gain - due to the movement of gut bacteria in to the blood stream and liver.

“Even in the absence of weight gain, fructose rapidly causes liver damage that we suggest is secondary to endotoxemia and microbial translocation,”​ commented the research team, led by Dr Kylie Kavanagh of Wake Forest Baptist Medical Center, USA.

"Based on our study findings, we can't say conclusively that fructose caused the liver damage,"​ explained Kavanagh. “What we can say is that high added sugars caused bacteria to exit the intestines, go into the blood stream and damage the liver.”

The researchers found that over the 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.

"What surprised us the most was how quickly the liver was affected and how extensive the damage was, especially without weight gain as a factor,"​ Kavanagh said. "Six weeks in monkeys is roughly equivalent to three months in humans."

Fructose damage?

The role of dietary fructose in the development of obesity and fatty liver diseases remains a controversial topic - with previous studies suggesting that the problems associated with fructose may be simply as a result of a higher calorific intake.

Previosu research from Kavanagh and her team studied monkeys who were allowed to eat as much as they wanted of low-fat food with added fructose for seven years, as compared to a control group fed a low-fructose, low-fat diet for the same time period.

Not surprisingly, the animals allowed to eat as much as they wanted of the high-fructose diet gained 50% more weight than the control group - they developed diabetes at three times the rate of the control group and also developed hepatic steatosis, or non-alcoholic fatty liver disease.

The big question for Kavanagh then, she said, was what caused the liver damage - was it because the animals got fat from eating too much, or was it something else like the fructose itself?

Study details

As a result, the new study in monkeys was designed to prevent weight gain. Ten middle-aged, normal weight monkeys who had never eaten fructose were divided into two groups based on comparable body shapes and waist circumference.

Over six weeks, one group was fed a calorie-controlled diet consisting of 24% fructose, while the control group was fed a calorie-controlled diet with only a negligible amount of fructose (approximately 0.5%).

Both diets had the same amount of fat, carbohydrate and protein, but the sources were different, Kavanagh said.

Every week the research team weighed both groups and measured their waist circumference, then adjusted the amount of food provided to prevent weight gain. At the end of the study, the researchers measured biomarkers of liver damage through blood samples and examined what type of bacteria was in the intestine through faecal samples and intestinal biopsies.

In the high-fructose group, the researchers found that the type of intestinal bacteria hadn't changed, but that they were migrating to the liver more rapidly and causing damage there.

“It appears that something about the high fructose levels was causing the intestines to be less protective than normal, and consequently allowing the bacteria to leak out at a 30% higher rate,” ​Kavanagh said.

"Is a calorie a calorie? Are they all created equal? Based on this study, we would say not,"​ she added.

‘Flawed’ study?

John W. Bode CEO and president of the US Corn Refiners Association commented that the authors of the ‘flawed’ study proves nothing about the cause of non-alcoholic fatty liver disease (NAFLD) in humans under real world conditions

“The AJCN study fails to reproduce anything close to resembling real world conditions for consuming fructose,”​ he said – noting that the primate subjects were fed pure fructose amounting to close to a quarter of the total calories consumed, which is over three times the average amount of fructose consumed from all sources in the human diet.

“Furthermore, HFCS and sugar are composed of roughly equal parts fructose and glucose.  Under no real world condition do people consume fructose alone and at such high levels.  This fact alone calls into question the credibility of the study.

“Attempts to demonise one food or ingredient without appropriate scientific research only lead to confusion among consumers and inhibit the development of real solutions.”  

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