Visit the Microscopic Colitis Foundation Website
I found this link to a table listing Glucose, Galactose, Fructose, Sucrose, Lactose, Maltose and Total metabolic fructose of fruits and sugars. Interestingly, it was on a Paleo Diet website:
http://www.thepaleodiet.com/nutritional ... table.html
This table might help determine an acceptable level of metabolic fructose for those of us who have trouble with fructose.
Gloria
Low Fructose Diet
Moderators: Rosie, Stanz, Jean, CAMary, moremuscle, JFR, Dee, xet, Peggy, Matthew, Gabes-Apg, grannyh, Gloria, Mars, starfire, Polly, Joefnh
Gloria,
That's a great reference table. Look at the dried fruits - drying really concentrates the sugars. They've got more sugar than most candy - not far below most of the pure sugars, on the average.
The diet police claim that sugar is strictly a modern addition to our diet, and therefore verboten, but obviously the paleo people ate a lot of sugar, too, because they routinely encountered dried fruits on and under trees, and ate them when all the fresh fruit was no longer available. Surely they were cleaver enough to figure out that fruits could be preserved for a while, by drying.
This suggests that, while we might react to sugars, something else is causing that sensitivity, rather than the sugars themselves.
Thanks for the link.
Tex
That's a great reference table. Look at the dried fruits - drying really concentrates the sugars. They've got more sugar than most candy - not far below most of the pure sugars, on the average.
The diet police claim that sugar is strictly a modern addition to our diet, and therefore verboten, but obviously the paleo people ate a lot of sugar, too, because they routinely encountered dried fruits on and under trees, and ate them when all the fresh fruit was no longer available. Surely they were cleaver enough to figure out that fruits could be preserved for a while, by drying.
This suggests that, while we might react to sugars, something else is causing that sensitivity, rather than the sugars themselves.
Thanks for the link.
Tex
It is suspected that some of the hardest material known to science can be found in the skulls of GI specialists who insist that diet has nothing to do with the treatment of microscopic colitis.
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faithberry
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faithberry
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Hedra, the list owner at the Yahoo Fructose Malabsorption Australia group posted this:
Faith
So NCGI is one of the underlying conditions for FM. I don't know what her references are but she does know a lot about FM.It is worth also testing for underlying conditions - celiac disease, non-celiac
gluten intolerance, food allergies, and SBBO or SIBO (small bowel bacterial
overgrowth) all can cause what is called 'secondary' Fructose Malabsorption.
Once those conditions are handled, and the bowel recovers from any injury
involved, more normal absorption of fructose can be gradually recovered.
Faith
Faith
LC (in remission)
LC (in remission)
Faith,
That observation follows from the fact that any form of enteritis causes a reduction in enzyme production in the brush border region of the small intestine. That's a well-established fact, that was documented long ago, and it's generally considered to be common knowledge, so no references should be needed. NCGS obviously causes enteritis.
In general, as the enteritis continues, and the inflammation increases, curtailment of the production of various enzymes that split the sugars, sequentially progresses. IOW, the first enzyme to go is lactase. I'm not sure what the exact order is, after that, but if the damage progresses sufficiently, virtually all enzyme production can be eventually severely diminished, which would, of course, also include the production of the enzymes necessary for the digestion of fructose, (whatever they are - I've never explored the process of fructose digestion).
When I was at my worst, (as far as sugar "tolerance" is concerned, I could handle maple sugar, and a small amount of fructose, (for example, I could drink 1 coke, but not two, in one day, without running into trouble), but I couldn't handle any other types of sugar, without getting sick.
Tex
That observation follows from the fact that any form of enteritis causes a reduction in enzyme production in the brush border region of the small intestine. That's a well-established fact, that was documented long ago, and it's generally considered to be common knowledge, so no references should be needed. NCGS obviously causes enteritis.
In general, as the enteritis continues, and the inflammation increases, curtailment of the production of various enzymes that split the sugars, sequentially progresses. IOW, the first enzyme to go is lactase. I'm not sure what the exact order is, after that, but if the damage progresses sufficiently, virtually all enzyme production can be eventually severely diminished, which would, of course, also include the production of the enzymes necessary for the digestion of fructose, (whatever they are - I've never explored the process of fructose digestion).
When I was at my worst, (as far as sugar "tolerance" is concerned, I could handle maple sugar, and a small amount of fructose, (for example, I could drink 1 coke, but not two, in one day, without running into trouble), but I couldn't handle any other types of sugar, without getting sick.
Tex
It is suspected that some of the hardest material known to science can be found in the skulls of GI specialists who insist that diet has nothing to do with the treatment of microscopic colitis.
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faithberry
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That makes sense. Fructose is a monosachharide (sp?) and thus does not require an enzyme for splitting. Technically, it's not digested. It uses a protein transporter called GLUT 5 in the enterocytes to move into the blood stream from the small bowel. In FM, it is thought there's a deficiency of the protein transporter due to inflammation or whatever. Sucrose needs to be split. Can't remember what sugars are in maple syrup, it seems to be better tolerated than most sugars.
In my mind, NCGS must cause enteritis in the small bowel but is that the position of medical doctors? They don't even believe in NCGS and from the recent John's Hopkins blurb they seem to happily tell people to keep eating gluten if they don't have the antibodies or damaged villi.
In my mind, NCGS must cause enteritis in the small bowel but is that the position of medical doctors? They don't even believe in NCGS and from the recent John's Hopkins blurb they seem to happily tell people to keep eating gluten if they don't have the antibodies or damaged villi.
Faith
LC (in remission)
LC (in remission)
Hmmmm. Yeah, it is a monosaccharide, isn't it. 
It's utilization is obviously somehow compromised, though, when enteritis is present.
NCGS causes the same type of inflammation in the small intestine, as it does in the colon, for many people with MC, but apparently this doesn't necessarily happen to everyone with MC. There are research articles online that verify this but I don't have the time to look any of them up, right now. If I recall correctly, some of Dr. fine's information posted on his website, also mentions that observation. People with celiac disease, in addition to MC, have both types of inflammation, (inflammation of the villi, resulting in villus atrophy, and intraepithelial lymphocytes, as in LC), Like Crohn's disease, MC can affect any part of the GI tract, from mouth to anus. The same type of inflammation can occur in the the stomach, esophagus, etc., but it most commonly affects the colon and small intestine.
You're right, mainstream doctors don't recognize small intestinal involvement, because the last part of the name for the disease, (colitis), applies only to the colon. (Doctors can be pretty hard-headed, and regimented, at times.). That's why Crohn's disease is usually referred to as Crohn's disease, rather than Crohn's colitis. Crohn's colitis is technically only correct if applied to cases where only the colon is involved. With ulcerative colitis, only the colon, (and downstream from there), is affected, and usually, only the distal colon, (since it always originates in the distal colon).
IOW, the name give to this disease, "microscopic colitis" was incorrect, right from the get-go. It's no wonder that most doctors are confused about the disease, since it was incorrectly described originally, and no one seems to know enough about it to even propose re-defining it, (if that's even legal, in the heavy-handed medical world).
Tex
It's utilization is obviously somehow compromised, though, when enteritis is present.NCGS causes the same type of inflammation in the small intestine, as it does in the colon, for many people with MC, but apparently this doesn't necessarily happen to everyone with MC. There are research articles online that verify this but I don't have the time to look any of them up, right now. If I recall correctly, some of Dr. fine's information posted on his website, also mentions that observation. People with celiac disease, in addition to MC, have both types of inflammation, (inflammation of the villi, resulting in villus atrophy, and intraepithelial lymphocytes, as in LC), Like Crohn's disease, MC can affect any part of the GI tract, from mouth to anus. The same type of inflammation can occur in the the stomach, esophagus, etc., but it most commonly affects the colon and small intestine.
You're right, mainstream doctors don't recognize small intestinal involvement, because the last part of the name for the disease, (colitis), applies only to the colon. (Doctors can be pretty hard-headed, and regimented, at times.
). That's why Crohn's disease is usually referred to as Crohn's disease, rather than Crohn's colitis. Crohn's colitis is technically only correct if applied to cases where only the colon is involved. With ulcerative colitis, only the colon, (and downstream from there), is affected, and usually, only the distal colon, (since it always originates in the distal colon).IOW, the name give to this disease, "microscopic colitis" was incorrect, right from the get-go. It's no wonder that most doctors are confused about the disease, since it was incorrectly described originally, and no one seems to know enough about it to even propose re-defining it, (if that's even legal, in the heavy-handed medical world).
Tex
It is suspected that some of the hardest material known to science can be found in the skulls of GI specialists who insist that diet has nothing to do with the treatment of microscopic colitis.
Faith,
You are right that fructose is a monsaccharide and the problem is with malabsorption not the enzyme/cleavingprocess - when fructose reaches the colon is fermets and causes gas, bloating and osmotic diarrhea. Fructose is part of disaccharide (sucrose) and also oligosaccharides (fructans). The problem with most low fructose diets is that they only focus on free fructose as a monosaccharide and forget that fructans in wheat and vegetables can cause the same symptoms. Sucrose is sometimes better tolerated than free fructose because the glucose tends to balance the fructose, but not always - many people on this forum have trouble with sucrose becasue of the osmotic effect. You can also have a problem with fructans in the colon as it undergoes rapid fermentation and has a huge osmotic effect. I recommend that anyone following a low fructose diet also assess if fructans are causing problems. I seem to have trouble with fructans in large quantities.
Mary Beth
You are right that fructose is a monsaccharide and the problem is with malabsorption not the enzyme/cleavingprocess - when fructose reaches the colon is fermets and causes gas, bloating and osmotic diarrhea. Fructose is part of disaccharide (sucrose) and also oligosaccharides (fructans). The problem with most low fructose diets is that they only focus on free fructose as a monosaccharide and forget that fructans in wheat and vegetables can cause the same symptoms. Sucrose is sometimes better tolerated than free fructose because the glucose tends to balance the fructose, but not always - many people on this forum have trouble with sucrose becasue of the osmotic effect. You can also have a problem with fructans in the colon as it undergoes rapid fermentation and has a huge osmotic effect. I recommend that anyone following a low fructose diet also assess if fructans are causing problems. I seem to have trouble with fructans in large quantities.
Mary Beth
Mary Beth,
Thanks for the hint. I think I may have figured it out.
Okay, so fructo-oligosaccharides consist of short chains of fructose molecules. These compounds can be only partially digested by humans, so when oligosaccharides are consumed, the undigested portion serves as food for “friendly” bacteria, such as Bifidobacteria and Lactobacillus species. In fact, oligosaccharides are sold as prebiotics, (not probiotics), specifically for that purpose. In the past, however, we've had discussions about whether it's just the good bacteria that benefit from such prebiotics, or all sorts of bacteria, and as a result, we've been reluctant to try prebiotics. IOW, thinking out loud here, it may be possible that if good bacteria are in short supply, then the undigested portion might give the "unfriendly" bacteria, the boost they need, to allow them to dig in and flex their muscles, and cause a balance that is barely holding it's own, to head south in a hurry.
IMO, though, the most likely scenario, involves lectins. Remember that lectins bind to specific carbohydrates, (oligosaccharides, to be exact), on mucosal cells, and act as an agglutinating agent, (which is the primary function of gluten, of course). Lectins can attach themselves to a specific receptor that is expressed on the gut wall, and pass through the intestinal barrier by that means, rather than through the tight junctions, through which legitimate nutrients pass. Therefore, the oligosaccharides provide them with a quick and dirty way to get into the bloodstream.
D-Mannose is looking better and better.
Tex
Thanks for the hint. I think I may have figured it out.
Okay, so fructo-oligosaccharides consist of short chains of fructose molecules. These compounds can be only partially digested by humans, so when oligosaccharides are consumed, the undigested portion serves as food for “friendly” bacteria, such as Bifidobacteria and Lactobacillus species. In fact, oligosaccharides are sold as prebiotics, (not probiotics), specifically for that purpose. In the past, however, we've had discussions about whether it's just the good bacteria that benefit from such prebiotics, or all sorts of bacteria, and as a result, we've been reluctant to try prebiotics. IOW, thinking out loud here, it may be possible that if good bacteria are in short supply, then the undigested portion might give the "unfriendly" bacteria, the boost they need, to allow them to dig in and flex their muscles, and cause a balance that is barely holding it's own, to head south in a hurry.
IMO, though, the most likely scenario, involves lectins. Remember that lectins bind to specific carbohydrates, (oligosaccharides, to be exact), on mucosal cells, and act as an agglutinating agent, (which is the primary function of gluten, of course). Lectins can attach themselves to a specific receptor that is expressed on the gut wall, and pass through the intestinal barrier by that means, rather than through the tight junctions, through which legitimate nutrients pass. Therefore, the oligosaccharides provide them with a quick and dirty way to get into the bloodstream.
D-Mannose is looking better and better.
Tex
It is suspected that some of the hardest material known to science can be found in the skulls of GI specialists who insist that diet has nothing to do with the treatment of microscopic colitis.
Tex,
That makes alot of sense. Sure wish lectins were being studied more. A book I just read by Jonathon Brostoff has also implicated lectins and mast cells in what he calls "false food allergy", or IOW why mast cells release mediators without true IgE allergies. D-mannose and the Paleo Diet are both looking good right now.
Mary Beth
That makes alot of sense. Sure wish lectins were being studied more. A book I just read by Jonathon Brostoff has also implicated lectins and mast cells in what he calls "false food allergy", or IOW why mast cells release mediators without true IgE allergies. D-mannose and the Paleo Diet are both looking good right now.
Mary Beth
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faithberry
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In fructose malabsorption, the problem isn't just feeding the baddies, but feeding the goodies (bacteria) too, as they also produce the gases that cause the symptoms. The issue is the bacteria getting too much to eat and producing too much of the gases, if I understand correctly, because fructose shouldn't be going into the colon generally speaking, it should be going into the blood stream. Fructo-O's do go there anyway so you don't want to be eating them if you already have too much fructose going into the wrong place. And polyols, if I understand correctly, compete for the fructose protein transporter sites. What I've learned so far!
Of course, lectins are another layer of possibility...
Of course, lectins are another layer of possibility...
Faith
LC (in remission)
LC (in remission)
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faithberry
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The reason that I am quite sure about having fructose malabsorption is due to having re-looked at my intestinal permeability test from 4+ years ago. The results showed that the mannitol uptake was very low, just on the border of abnormal. This indicates malabsorption of small molecules (like fructose). The mannitol/lactulose ratio was also high, which can indicate leaky gut in some cases, especially in gluten sensitive enteropathy in which both leaky gut and malabsorption of small molecules can occur simultaneously.
Although I had already eliminated wheat and the obvious forms of gluten, it was still one year before I eliminated all traces of gluten plus casein too. Not to mention other intolerances that emerged like corn. So in that year, it's likely to have gotten worse, not better.
After giving up gluten, I thought I was home-free because the D. stopped, but I was never able to regain my ability to eat a normal diet. In the process of trying to eat more foods in the last three years and then my recent encounters with brown rice and millet, I've just gotten worse again.
For me, it looks like paleo without the red meat, fish, vegetables, fruits or nuts but a deviation for white rice:-), but at least I understand now.
Although I had already eliminated wheat and the obvious forms of gluten, it was still one year before I eliminated all traces of gluten plus casein too. Not to mention other intolerances that emerged like corn. So in that year, it's likely to have gotten worse, not better.
After giving up gluten, I thought I was home-free because the D. stopped, but I was never able to regain my ability to eat a normal diet. In the process of trying to eat more foods in the last three years and then my recent encounters with brown rice and millet, I've just gotten worse again.
For me, it looks like paleo without the red meat, fish, vegetables, fruits or nuts but a deviation for white rice:-), but at least I understand now.
Faith
LC (in remission)
LC (in remission)
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faithberry
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I think this is one of the best explanations of fructose malabsorption and the FODMAPs diet (including fructans and polyols).
http://www.healthhype.com/fructose-mala ... nosis.html
When you get to the end of the page, there are 2 links, one to Safe/Unsafe food list and diet information and the other to a chart that lists all the foods with excess glucose, fructans, and polyols. Of course, food lists vary depending on the source and location (because fructose content varies), but this is quite a good one.
http://www.healthhype.com/fructose-mala ... nosis.html
When you get to the end of the page, there are 2 links, one to Safe/Unsafe food list and diet information and the other to a chart that lists all the foods with excess glucose, fructans, and polyols. Of course, food lists vary depending on the source and location (because fructose content varies), but this is quite a good one.
Faith
LC (in remission)
LC (in remission)
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faithberry
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Tex,
You said...
I have a question for you in response to your point:
If the intraepithelial lymphocytes occur in celiac disease too,how do they differentiate it from LC in small bowel, aside from atropy of the villi?
Hope that makes sense.
Thanks!
You said...
Yes, I don't disagree with that point at all!!!!!Hmmmm. Yeah, it is a monosaccharide, isn't it. Laughing Rolling Eyes It's utilization is obviously somehow compromised, though, when enteritis is present.
I have a question for you in response to your point:
When I had my upper endoscopy done they checked for celiac disease and for whipple's disease. Does that mean they could have missed intraepithelial lymphocytes if they didn't check for them specifically? The results say: "do not see atrophy or inflammatory changes of sprue" so does the latter "inflammatory changes of sprue" mean intraepithelial lymphocytes as one would also see in lymphocytic "colitis" in the small bowel though?NCGS causes the same type of inflammation in the small intestine, as it does in the colon, for many people with MC
If the intraepithelial lymphocytes occur in celiac disease too,how do they differentiate it from LC in small bowel, aside from atropy of the villi?
Hope that makes sense.
Thanks!
Faith
LC (in remission)
LC (in remission)