Thanks to Jamie Scott and Melchior Meijer (PolderPaleo) for an interesting discussion about this hypothesis. This embedded tweet should get to you to the entire discussion, if you're interested.@TuckerGoodrich @PolderPaleo Not really beat you to it. Suggestion to put your critique directly to Spreadbury still holds.— Jamie Scott (@_Jamie_Scott) November 13, 2016
Sunday, November 13, 2016
Thoughts on Spreadbury's "Cellular Carbohydrate" Hypothesis
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Hi Tucker,
ReplyDeleteThanks a lot for this thorough analysis.
I have to admit that the distinction between cellular and acellular falls apart. But in my mind this has never been the core of the concept. The core of the concept - as I see it - is that 'ancestral' foods, even if cooked, have such a low starch density per swallowed unit that they are not able to serve as a substrate for the microbiome in the upper small intestine (SI). Even if the walls of a tuber are distroyed by cooking, which they most ofte are as you pointed out, the absolute amount of starch reaching the SI will be lower after each swallow, than it would be after consuming, say, bread or pasta or any grain product, which are very dense. The GI of a cooked tuber is high, but since the amount of starch is limited, it will be almost immediately hydrolized and absorbed into the circulation. This is critcal in my view. At any given moment there will not be enough substrate in the upper SI to create or sustain a toxic microbiome. As soon as the amount of starch per bolus of chyme exceeds the capacity of the enzymes to hydrolyze it into glucose, there will be a time window in which the starch can be substrate for the flora. As to pure glucose, only small amounts, such as found in whole fruit, are safe. Glucose becomes a problem if the concentration is higher than can be immediately absorbed into the circulation, for the very same reason that in that case it becomes substrate for the flora.
In this respect Spreadbury's hypothesis is entirely different than the falsified fiber hypothesis by Burkitt and Trowell. Adding fiber to very dense starch sources like grain products will do almost nothing to the starch load the upper SI will see. If anything, the fiber will serve as an extra substrate to feed into an already toxic upper intestinal soup, especially when transit time is altered.
In a way I see Spreadbury's hypothesis as a neat explanation for why fiber free (all meat) diets turn out to be so tremendously effective against a plethora of ailments. Any diet that doesn't deliver a high load of substrate to the SI-microbiome, will produce health, I think. I'm not at all saying that tubers are necessary for or even contributing to good health, only that the absolute amount of starch they dump into our gut might be just low enough to not create problems. This would explain a lot of seemingly paradoxical observations.
So far my first thoughts. Thanks again for creating this opportunity to discuss this concept!
Melchior. (PolderPaleo :-) )
1. I can't help wondering how this cooking of tubers to acellularity is related to resistant versus non-resistant starch, for example when a potato is cooked and then cooled which supposedly makes (some of) the starch resistant again. And then there's soluble versus insoluble fiber. Are these all different names for the same thing?
ReplyDelete2. Here's a really dumb question: why is it so hard to determine whether cooking breaks down cell walls—can't this be seen under a microscope? Looks like they may have done it here, although this was a study on repeated cooking and cooling cycles involving resistant starch: https://pubmed.ncbi.nlm.nih.gov/19562607/
3. Another way of processing food is fermentation, as in fermented vegetables such as sauerkraut. I'm getting ready to ferment some raw potatoes, for example.
Regarding 2: the best way to determine if cell walls are being broken in vivo is blood glucose. It tells you if in fact the glucose behind the cell wall is making it into the blood, which is what we care about.
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