tyw
Member
Interesting post but my personal experience was the exact opposite if this. When I ate a zero fat diet with only a Tiny amount of of CO, I got sever endotoxin shock reactions. Now that I eat zero fiber, zero starch and a lot of saturated fat I get zero endotoxin symptoms, it's like night and day.
The biggest thing I think is how much endotoxin is in the gut in the first place. Carbs will almost certainly contribute more to feeding bacteria and producing way more endotoxin, also it will create fermentaton which will cause the digestive tract to expand and become more leaky. Lastly, what about the saturated fat that is produced in the large intestine? Could this cause the same reaction as dietary saturated fat?
Yes, your experience is consistent with all the mechanisms I stated :) . Fat can only transport existing endotoxin in the small intestine to the rest of the body. If there is no endotoxin to begin with, then there is nothing to transport.
Now we need to qualify what your "zero fat diet" meant. The mechanisms of:
- chylomicrons transporting endotoxin from the small intestine to the rest of the body
- production of endotoxin by bacteria in the small intestine.
Are completely separate from each other.
This is why I said many times that "zero fat" doesn't mean anything for endotoxin risk. A "zero fat" diet with fermentable materials like pectin or FODMAPS is still a breeding ground for bacteria which can produce endotoxin.
The control experiment would be zero fat, zero fermentable carbohydrate. This is not an easy practical experiment to run, and involves a decent amount of food control. (Sidenote: that said, my regular diet is basically zero fermentable carbohydrates , and very low fat)
Even then, the definition of a "fermentable carbohydrate" can be murky. For me, pure amylopectin basically just gets absorbed very quickly -- I lose the feeling of fullness very quickly, blood sugar spikes very quickly, and recovers to baseline very quickly ("very quickly" meaning like 2-3 hours for even a 2,000kcal meal). All indications of gut health seem to indicate that this is not going to give bacteria the opportunity for fermentation.
High Amylose on the other hand, gives me issues with bloating. No basmati rice please! (Just search "tyw rice" for my previous posts elaborating on these topics in detail)
All you can do with these mechanics, is to understand them, and then think about future experiments.
And lastly (and IMPORTANTLY ) do note that the small intestine is a very high turnover system -- border cells which only last for a few days. This makes the response to a particular molecule very different as "conditions of existence" change. For someone with a history of gut issues, constant monitoring and constant tweaking is required, and the assumption that "what works today will work tomorrow" is not valid.
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This chylomicron-mediated endotoxin transport mechanism does not come into play at all in the large intestine. There, we have to look at other factors, like butyrate production by bacteria (which is likely beneficial as far as I can tell).
Large intestine bacterial populations are something which needs to be discussed in a separate thread, with research and mechanics specific to that.
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