“After reading the research reviewed in that post, I'm quite convinced that the development of fatty liver is pretty simple: anything that increases the amount of energy that the liver needs to process forms the first part; anything that impairs the ability of the liver to export that energy forms the second part. High intakes of total calories, sugar, fat, or alcohol can all contribute to fatty liver in animals. But the king of all nutrients needed to export that energy as fat, choline, protects against the disease in all of these animal models.
Of course, a high intake of PUFA contributes to the inflammatory component, and when combined with other toxic factors may also contribute to the fatty component by preventing the liver from exporting its fat.”
Does Choline Deficiency Contribute to Fatty Liver in Humans | Chris Masterjohn, PhD
If you keep fructose below 1 g/kg, it should not even reach the liver.
“High doses of fructose (≥1 g/kg) overwhelm intestinal fructose absorption and clearance, resulting in fructose reaching both the liver and colonic microbiota. Intestinal fructose clearance is augmented both by prior exposure to fructose and by feeding. We propose that the small intestine shields the liver from otherwise toxic fructose exposure.”
The Small Intestine Converts Dietary Fructose Into Glucose And Organic Acids
“Fructose consumption at moderate levels of intake do not adversely effect body weight or blood chemistry based on the current data. Obscenely high levels of intake (>150 grams per day) may have undesirable health effects”
Fructose: Burying the Boogeyman - Science Driven Nutrition
This is one of my issues with health forums in general, when someone shares an experience that contradicts the forum, then someone throws a load of studies of them to prove them wrong.
I developed fatty liver diagnosed by ultrasound after eating a Peat inspired diet, very similar to ones on here, it doesn't matter how many studies I read about it. I never had this issue before discovering Peat.