Question about fructose that I can’t find an answer to:
When fructose breaks down in the small intestine, *before it reaches the liver*, are the breakdown process and its byproducts damaging/toxic (like they are in the liver) or are they innocuous?
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Chaffee says fructose breaks down into ethanol and does damage post metabolization.
Thanks but this doesn’t address my question and I already acknowledged the liver in my post. This is about the breakdown in the small intestine first. You can learn about that process here https://m.youtube.com/watch?v=rIR8n6yFKDw
Interesting. I wonder how much fruit it would take to exceed fructose filtering capacity. Modern selectively bred fruit contains a lot of fructose.
Here he breaks down an upper limit of 0.25g-0.5g/kg bodyweight / day before the fructose spills over to the portal vein. For a 165lb person, that’s ~20-40g/day, which isn’t much. He’s also transparent about the limitations of that study and the nuance of that upper limit recommendation. https://m.youtube.com/watch?v=QjJr5qvRkBk
Wow so very minimal mitigation. Fruit enjoyers rekt.
Oh boy, you just sent me down a new rabbit hole. Thank you.
After reading a single paper of which I only understood half, it seems like low amounts are fine but high amounts can lead to all sorts of bad stuff, even in the intestine.
2.2. Fructose and Intestine
Under normal intestinal conditions, fructose has the same metabolic fate in the form of sucrose or fructose alone [13,68]. Fructose carbons are rapidly converted to glucose, glycerate, and TCA metabolites within enterocytes, the primary cell type within the intestine. These byproducts are typically shuttled through the portal vein to the liver for further processing and metabolism. In enterocytes, fructose is converted to fructose-1-phosphate by KHK (Figure 1). Elevated intracellular levels of fructose-1-phosphate can be toxic, leading to endoplasmic reticulum stress and inflammation, which is reported to induce barrier deterioration and shorten colon length [84]. Taylor et al. discovered that fructose promotes hypoxic cell survival via extended villi length, partly through fructose-1-phosphate inhibition of the hypoxic adaptation protein pyruvate kinase isozyme M2 (PKM2) [85]. The extension of the length of the villi increased weight gain, nutritional absorption, and fat accumulation. High levels of fructose lead to a misshapen colon and cecum as well as infiltration of inflammatory macrophages, neutrophils, dendritic cells, and natural killer T cells into the lamina propria. These cells express the inflammatory cytokines interleukin 1 beta (IL-1β), interleukin 2 (IL-2), and interleukin 6 (IL-6) within the small intestine of mice [86,87]. In addition, cecal metabolites such as prostaglandin B1 and I2, which are important for regulating blood pressure, inflammation, and fibrosis, are elevated in male mice on a fructose diet [88]. Although fructose metabolism begins within the small intestine at low doses, it can bypass initial metabolism at higher doses and be shuttled through the portal vein for further processing [89].
A bit of a segue. Considering all the emerging negative aspects of high fructose corn syrup, the Netflix “King Corn” documentary should scare the living crap out of us.
