The medical profession has overlooked some major pathological effects of fructose consumption and its effects on liver function. Regardless of whether or not a person gains weight from it, consuming fructose was recently shown by researchers from Wake Forest Baptist Medical Center in North Carolina to cause hepatic steatosis, a non-alcoholic form of fatty liver disease that in some patients can lead to cirrhosis.
Published in the American Journal of Clinical Nutrition (AJCN), their study found that, by itself, fructose can trigger rapid liver damage even when all other factors remain equal. In other words, a relatively skinny person can sustain extensive liver damage from fructose consumption, even if he or she doesn’t become obese from it. Fructose consumers also have an exceptional propensity toward developing diabetes, according to the data.
“Is a calorie a calorie? Are they all created equal? Based on this study, we would say not,” said Kylie Kavanagh, D.V.M., an assistant professor of pathology and comparative medicine at Wake Forest Baptist Medical Center, and lead author of the study. “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.”
For their research, scientists gave two groups of monkeys an all-you-can-eat buffet for seven years. The target group was given access to low-fat foods with added fructose, while the control group was given access only to low-fat, low-fructose foods. All other factors remained equal, and the animals were given equal access to whatever quantities of food they desired.
During the evaluative period, monkeys in the fructose group were observed to gain about 50 percent more weight than the control group. They also developed diabetes at three times the rate of the control group as well as severe cases of hepatic steatosis that were clearly unique to fructose consumption.
Fructose shown to damage intestinal flora, cause gut leakage
In order to verify that fructose itself, and not some combination of fructose and weight gain, was responsible for the high rates of liver damage, the researchers took 10 middle-aged, normal-weight monkeys who had never before consumed fructose and divided them into two comparable groups. Both groups of monkeys had similar body shapes and waist circumferences.
For a course of six weeks, one group was fed a calorie-controlled diet containing 24 percent fructose while the other group was fed a calorie-controlled diet containing a negligible amount of fructose, or about 0.5 percent. Both groups were given an equal amount of fat, carbohydrates and protein, but from varying sources.
The high-fructose diet contained flour, butter, pork fat and eggs, while the low-fructose diet contained complex carbohydrates and soy protein — these combinations were assigned to ensure that both groups of monkeys remained at a similar weight. After six weeks on the two regimens, blood samples were collected to look for biomarkers of liver damage, as well as to assess bacterial composition in the monkeys’ guts.
What they found is that not only did fructose directly harm the monkeys’ livers, but it also altered the bacterial composition of their guts. In essence, fructose was found to cause intestinal microflora to leak from the intestines, enter the bloodstream and damage the liver — and at a rate of up to 30 percent higher compared to the monkeys that consumed almost no fructose.
“High added sugars caused bacteria to exit the intestines, go into the blood stream and damage the liver,” wrote the authors. “The liver damage began even in the absence of weight gain. This could have clinical implications because most doctors and scientists have thought that it was the fat in and around tissues in the body that caused the health problems.”
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