Dietary fructose causes liver damage in monkeys:
In a previous trial which is referenced in the current journal article, Kavanagh’s 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 percent 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 the researchers was what caused the liver damage. Was it because the animals got fat from eating too much, or was it something else?
To answer that question, this study 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 percent fructose, while the control group was fed a calorie-controlled diet with only a negligible amount of fructose, approximately 0.5 percent.
Both diets had the same amount of fat, carbohydrate and protein, but the sources were different, Kavanagh said. 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.
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 fecal samples and intestinal biopsies.
“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.”
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 percent higher rate, Kavanagh said.
But if they were trying to isolate the effects of fructose, why did treatment and control vary in diets so broadly in the last bit?
Yeah, it’s a bit odd to compare flour, butter, pork fat, eggs and fructose against complex carbs and soy protein and conclude that the difference came down to fructose.
I found it odd that monkeys had any trouble with fructose, since they’re known for eating fruit.
Mainstream nutrition theory is so far from reality that the experiments it designs don’t have any value at all.
Problems with this experiment:
1) “Fat” isn’t just one thing.
2) Proteins aren’t interchangeable; they’re freaking complex chemicals that have effects when ingested.
3) “Eggs” aren’t just one thing. Were they fed real eggs or spray dried reconstituted eggs? Eggs from pastured chickens? These things change the makeup of the egg. An “egg” isn’t an interchangeable thing.
4) “Complex carbs” aren’t a thing either. Were they wheat? Wheat has all sorts of effects that cause autoimmune reactions.
Basically their model is so far off that they can’t even build an experiment because the assumptions are so bad.
One might say there is no such thing as a macronutrient.
Excellent post at the link which cuts right to the heart of the confusion of the experiment discussed in this post.