Are IgA chicken egg antibodies to the yolk or white or both?
Moderators: Rosie, Stanz, Jean, CAMary, moremuscle, JFR, Dee, xet, Peggy, Matthew, Gabes-Apg, grannyh, Gloria, Mars, starfire, Polly, Joefnh
Are IgA chicken egg antibodies to the yolk or white or both?
We recently bit the bullet and had my daughter tested through Enterolab. I knew she had dairy problems and seemed to have gluten problems as well (though she hasn't had much of either since we are a gluten free house and only have cheese and butter for dairy)
Anyway, I was blown away by her results! She was 106 for gluten 37 for both dairy and eggs, and 49 for soy. To make matters worse she has a double Celiac gene-201 and 302 (we had no idea until now that my husband carried a Celiac gene).
So now I am so scattered trying to figure out how to make things with almond flour without eggs! (we have gone mostly grain free with the kids since my oldest has diabetes and the nut flours are much more blood glucose stabilizing)
To my question....has anyone who tested positive for antibodies to chicken eggs figured out if it is the egg white, the egg yolk, or both? I just don't know enough about this. Do the whites and yolks carry the same protein? Thanks for the help! Susie
Anyway, I was blown away by her results! She was 106 for gluten 37 for both dairy and eggs, and 49 for soy. To make matters worse she has a double Celiac gene-201 and 302 (we had no idea until now that my husband carried a Celiac gene).
So now I am so scattered trying to figure out how to make things with almond flour without eggs! (we have gone mostly grain free with the kids since my oldest has diabetes and the nut flours are much more blood glucose stabilizing)
To my question....has anyone who tested positive for antibodies to chicken eggs figured out if it is the egg white, the egg yolk, or both? I just don't know enough about this. Do the whites and yolks carry the same protein? Thanks for the help! Susie
Susie,
Wow! Good thing you caught this early.
Since most people who are sensitive to eggs are sensitive to the primary protein in the albumen (the white), that is the one for which the EnteroLab egg test was developed. There are other proteins in the albumen that are not tested for, and the yolk contains it's own proteins (that no test is available for).
The problem with your plan is that I'm not aware of any tests that are available anywhere, to test for any of the proteins in the egg yolk. And just because no test is available does not mean that she (or anyone else) could not be sensitive to one or more of the proteins in the yolk.
That said, it's also certainly possible that she might be able to tolerate the yolk — we just have no test to determine that. The other problem is obtaining complete separation of the albumen and the yolk. In baked goods, though, many members here seem to be able to tolerate reasonable amounts of eggs, so as long as you get normal separation, that might be adequate (if egg yolks will provide the baking characteristics needed as a binder.) Yolks carry slightly more than half the total amount of protein found in an egg, but of course it's different proteins than the ones found in the albumen.
If I remember correctly, Gloria has become an expert on cooking with almond flour.
Tex
Wow! Good thing you caught this early.
Since most people who are sensitive to eggs are sensitive to the primary protein in the albumen (the white), that is the one for which the EnteroLab egg test was developed. There are other proteins in the albumen that are not tested for, and the yolk contains it's own proteins (that no test is available for).
The problem with your plan is that I'm not aware of any tests that are available anywhere, to test for any of the proteins in the egg yolk. And just because no test is available does not mean that she (or anyone else) could not be sensitive to one or more of the proteins in the yolk.
That said, it's also certainly possible that she might be able to tolerate the yolk — we just have no test to determine that. The other problem is obtaining complete separation of the albumen and the yolk. In baked goods, though, many members here seem to be able to tolerate reasonable amounts of eggs, so as long as you get normal separation, that might be adequate (if egg yolks will provide the baking characteristics needed as a binder.) Yolks carry slightly more than half the total amount of protein found in an egg, but of course it's different proteins than the ones found in the albumen.
If I remember correctly, Gloria has become an expert on cooking with almond flour.
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.
Thank you Tex, That is very helpful.
My daughter is three and she was diagnosed with milk protein intolerance pretty much at birth. I have been fairly concerned for my kids considering that I did not know about my intolerances when pregnant and nursing, and from deduction I have figured I passed on my intolerances to them (I know IgA antibodies are passed through breastmilk). I have three kids with known Celiac/Diabetes genes, and my first has type I diabetes since age 1. It is my own personal belief that gluten and milk proteins combined with antibodies and disrupted gut bacteria may be the trigger for type I diabetes. Trying to spare them devastating diseases later in life!!!
Thanks again. I think I will try the banana substitution for egg for a while and then maybe see if she can handle the yolk!
Susie
My daughter is three and she was diagnosed with milk protein intolerance pretty much at birth. I have been fairly concerned for my kids considering that I did not know about my intolerances when pregnant and nursing, and from deduction I have figured I passed on my intolerances to them (I know IgA antibodies are passed through breastmilk). I have three kids with known Celiac/Diabetes genes, and my first has type I diabetes since age 1. It is my own personal belief that gluten and milk proteins combined with antibodies and disrupted gut bacteria may be the trigger for type I diabetes. Trying to spare them devastating diseases later in life!!!
Thanks again. I think I will try the banana substitution for egg for a while and then maybe see if she can handle the yolk!
Susie
Susie,
Did you see the quote that I posted for another member, concerning the development of diabetes?
4. Visser, J., Rozing, J., Sapone, A., Lammers, K., & Fasano, A. (2009). Tight junctions, intestinal permeability, and autoimmunity: celiac disease and type 1 diabetes paradigms. Annals of the New York Academy of Sciences, 1165(1), 195–205. doi:10.1111/j.1749-6632.2009.04037.x
34. Carratù, R., Secondulfo, M., de Magistris, L., Iafusco, D., Urio, A., Carbone, M. G., . . . Prisco, F. (1999). Altered intestinal permeability to mannitol in diabetes mellitus type I. Journal of Pediatric Gastroenterology & Nutrition, 28(3), 264–269. Retrieved from http://journals.lww.com/jpgn/Fulltext/1 ... in.10.aspx
35. Fasano, A., Watts, T., Sapone, A., & Zielke, R. (2004). P0086 Pp Zonulin-Dependent Increased Intestinal Permeability Is Involved in the Pathogenesis of Type 1 Diabetes and Can Be Blocked to Prevent the Onset of the Disease. Journal of Pediatric Gastroenterology & Nutrition, 39(1), S89–S90. Retrieved from http://journals.lww.com/jpgn/Fulltext/2 ... l.210.aspx
36. Geoffrey, R., Jia, S., Kwitek, A. E., Woodliff, J., Ghosh, S., Lernmark, A., . . . Hessner, M. J. (2006). Evidence of a functional role for mast cells in the development of type 1 diabetes mellitus in the biobreeding rat. The Journal of Immunology, 177(10), 7275–7286.Retrieved from http://www.jimmunol.org/content/177/10/7275.full
37. Liu, J., Divoux, A., Sun, J., Zhang, J., Clément, K., Glickman, J. N., . . . Shi, G-P. (2009). Genetic deficiency and pharmacological stabilization of mast cells reduce diet-induced obesity and diabetes in mice. Nature Medicine, 15(8), 940–945. doi:10.1038/nm.1994
38. Lloyd, C., Smith, J., & Weinger, K. (2005). Stress and diabetes: A review of the links. Diabetes Spectrum, 18(2), 121–127. doi:10.2337/diaspect.18.2.121
39. Wellen, K. E., & Hotamisligil, G. S. (2005). Inflammation, stress, and diabetes. Journal of Clinical Investigation, 115(5), 1111–1119. doi:10.1172/JCI200525102
You're very welcome,
Tex
Did you see the quote that I posted for another member, concerning the development of diabetes?
That quote is from chapter 16 of my book, and here are the references associated with it:Research done as far back as 1997 and published in 1999 showed that type 1 diabetes is clearly associated with increased intestinal permeability.34 Research data that were published in 2004 showed that type 1 diabetes could be prevented simply by eliminating or preventing increased intestinal permeability.35 In 2009, research revealed that one or more of the peptides in the gluten molecule appears to be a factor in the development of type 1 diabetes, and Visser et al. (2009) hypothesized that increased intestinal permeability is essential to the development of autoimmune disease.4 Clearly, if it can be validated, that’s a very profound observation, with far-reaching implications.
So now we have to ask, “Are mast cells also involved in the development of diabetes mellitus?” And the answer, of course, is “Yes”. While experiments with human subjects haven’t been done, research using rats and mice clearly shows that mast cells are involved in the development of diabetes.36, 37 It's well known that Type 1 diabetes is associated with gluten-sensitive enteropathy, so the discovery of a mast cell connection is a logical extension of that association, given the information in this chapter. Research done by Liu et al. (2009) suggests that obesity can even be reduced by using a treatment to stabilize mast cells, to prevent their inappropriate degranulation.37
And other research shows that the final link, stress, is clearly implicated as a factor that drives blood sugar excursions that can lead to insulin resistance and the development of diabetes.38, 39 In addition, Wellen and Hotamisligil (2005) discuss mechanisms by which inflammation may lead to obesity, and this was verified by Liu et al. (2009), as mentioned above. The bottom line is that all of the components of my theory are present in the development of diabetes mellitus.
4. Visser, J., Rozing, J., Sapone, A., Lammers, K., & Fasano, A. (2009). Tight junctions, intestinal permeability, and autoimmunity: celiac disease and type 1 diabetes paradigms. Annals of the New York Academy of Sciences, 1165(1), 195–205. doi:10.1111/j.1749-6632.2009.04037.x
34. Carratù, R., Secondulfo, M., de Magistris, L., Iafusco, D., Urio, A., Carbone, M. G., . . . Prisco, F. (1999). Altered intestinal permeability to mannitol in diabetes mellitus type I. Journal of Pediatric Gastroenterology & Nutrition, 28(3), 264–269. Retrieved from http://journals.lww.com/jpgn/Fulltext/1 ... in.10.aspx
35. Fasano, A., Watts, T., Sapone, A., & Zielke, R. (2004). P0086 Pp Zonulin-Dependent Increased Intestinal Permeability Is Involved in the Pathogenesis of Type 1 Diabetes and Can Be Blocked to Prevent the Onset of the Disease. Journal of Pediatric Gastroenterology & Nutrition, 39(1), S89–S90. Retrieved from http://journals.lww.com/jpgn/Fulltext/2 ... l.210.aspx
36. Geoffrey, R., Jia, S., Kwitek, A. E., Woodliff, J., Ghosh, S., Lernmark, A., . . . Hessner, M. J. (2006). Evidence of a functional role for mast cells in the development of type 1 diabetes mellitus in the biobreeding rat. The Journal of Immunology, 177(10), 7275–7286.Retrieved from http://www.jimmunol.org/content/177/10/7275.full
37. Liu, J., Divoux, A., Sun, J., Zhang, J., Clément, K., Glickman, J. N., . . . Shi, G-P. (2009). Genetic deficiency and pharmacological stabilization of mast cells reduce diet-induced obesity and diabetes in mice. Nature Medicine, 15(8), 940–945. doi:10.1038/nm.1994
38. Lloyd, C., Smith, J., & Weinger, K. (2005). Stress and diabetes: A review of the links. Diabetes Spectrum, 18(2), 121–127. doi:10.2337/diaspect.18.2.121
39. Wellen, K. E., & Hotamisligil, G. S. (2005). Inflammation, stress, and diabetes. Journal of Clinical Investigation, 115(5), 1111–1119. doi:10.1172/JCI200525102
You're very welcome,
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.
Wow! I have never seen this! I guess my hunches were on the right track! I have another quick question for you. I have been reading a lot about diabetes in the last day, and one thing I never knew is that I am continually creating antibodies to insulin. Do you think that one of the reasons I am having trouble achieving remission is that since I take exogenous insulin and continually produce antibodies toward insulin, my body is in a hyper immune state. (I can't remove the insulin and thus the antibodies toward it) I mean it is ridiculous righ now! I caught another cold, and am eating only buffalo, carrots, zucchini and duck and I am still a mess! Realized I can't even eat butternut squash. I had read something that said before you can get your body to stop attacking itself you have to remove the root trigger. Well I can't remove insulin! Just curious as to your thoughts on that theory! Thanks again for that info! More helpful than you could know!
Susie,
I believe that most people who take insulin (probably everyone who takes it) produces antibodies to it. That just means that your immune system is working correctly, because (as you pointed out) supplemental insulin is an exogenous agent, and therefore as far as your immune system is concerned, it's a foreign substance, so it is naturally going to produce antibodies to it.
I don't know this for a fact (because I've never actually looked for it), but I'm pretty sure that the official medical position on this is that it doesn't matter. And even if it does matter, as you are well aware, there's not much anyone can do about it. As far as utilizing the insulin is concerned, it still seems to do the job.
However, if you're familiar with my theory that the immune system tends to concentrate on whatever it considers to be the single biggest health threat at the moment, then it's easy to visualize how your immune system may be wasting it's efforts on supplemental insulin (which it can't really do anything about), while ignoring it's obligations to protect your body from cold viruses, or similar problems. In your case, though, it seems to be concentrating its efforts on your food sensitivities.
Of course, for all we know, the immune system may continue to produce high levels of antibodies against any antigens that enter the body, but it only actually acts on those that are considered to be at the top of the hierarchy. I doubt that this has ever been researched, but if that turns out to be the case, then the high antibody level against insulin would be pretty much irrelevant, because your immune system is concentrating it's efforts on your food sensitivities, instead.
If this is true, then it would expand on my theory (and enhance it) to allow for the fact that the immune system does indeed produce antibodies to all perceived antigens, but as I've always claimed, it only launches an actual attack against the threat considered to be the most important, at any given time. This addition makes sense, and IMO it's very likely to be true (but obviously it's unproven by any medical research).
Many people eventually develop a tolerance for food sensitivities. For example, I can tolerate casein, but I produce antibodies to it, so I avoid it. Some celiacs become tolerant of gluten (but they still produce antibodies to it, and in many cases, small intestinal damage continues to accrue. I have no idea though, if anyone ever develops a tolerance to insulin, but I would assume that it's certainly a possibility, otherwise people who have no other distractions for their immune system, might suffer a severe immune system reaction.
So the bottom line is, it may be possible that even though your immune system may be producing a high level of antibodies against insulin, it may not matter, because you have developed a tolerance for it. And even if you haven't, the question of whether or not the production of antibodies against insulin adds to any relative degree of hypersensitivity may be a moot point, because your immune system seems to be devoting all it's actual efforts against food sensitivities.
I hope that someone decides to research this concept some day, because it could answer a lot of important questions about the way our immune system works.
Tex
I believe that most people who take insulin (probably everyone who takes it) produces antibodies to it. That just means that your immune system is working correctly, because (as you pointed out) supplemental insulin is an exogenous agent, and therefore as far as your immune system is concerned, it's a foreign substance, so it is naturally going to produce antibodies to it.
I don't know this for a fact (because I've never actually looked for it), but I'm pretty sure that the official medical position on this is that it doesn't matter. And even if it does matter, as you are well aware, there's not much anyone can do about it. As far as utilizing the insulin is concerned, it still seems to do the job.
However, if you're familiar with my theory that the immune system tends to concentrate on whatever it considers to be the single biggest health threat at the moment, then it's easy to visualize how your immune system may be wasting it's efforts on supplemental insulin (which it can't really do anything about), while ignoring it's obligations to protect your body from cold viruses, or similar problems. In your case, though, it seems to be concentrating its efforts on your food sensitivities.
Of course, for all we know, the immune system may continue to produce high levels of antibodies against any antigens that enter the body, but it only actually acts on those that are considered to be at the top of the hierarchy. I doubt that this has ever been researched, but if that turns out to be the case, then the high antibody level against insulin would be pretty much irrelevant, because your immune system is concentrating it's efforts on your food sensitivities, instead.
If this is true, then it would expand on my theory (and enhance it) to allow for the fact that the immune system does indeed produce antibodies to all perceived antigens, but as I've always claimed, it only launches an actual attack against the threat considered to be the most important, at any given time. This addition makes sense, and IMO it's very likely to be true (but obviously it's unproven by any medical research).
Many people eventually develop a tolerance for food sensitivities. For example, I can tolerate casein, but I produce antibodies to it, so I avoid it. Some celiacs become tolerant of gluten (but they still produce antibodies to it, and in many cases, small intestinal damage continues to accrue. I have no idea though, if anyone ever develops a tolerance to insulin, but I would assume that it's certainly a possibility, otherwise people who have no other distractions for their immune system, might suffer a severe immune system reaction.
So the bottom line is, it may be possible that even though your immune system may be producing a high level of antibodies against insulin, it may not matter, because you have developed a tolerance for it. And even if you haven't, the question of whether or not the production of antibodies against insulin adds to any relative degree of hypersensitivity may be a moot point, because your immune system seems to be devoting all it's actual efforts against food sensitivities.
I hope that someone decides to research this concept some day, because it could answer a lot of important questions about the way our immune system works.
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.
Susie,
The double celiac genes had to come as quite a shock. Will your husband go GF, too, or is he already?
Gloria
The double celiac genes had to come as quite a shock. Will your husband go GF, too, or is he already?
I make muffins, pancakes, and waffles without eggs using almond flour, corn flour, cornstarch, arrowroot flour and homemade almond milk. I've posted the recipes in Dee's Kitchen. It's not Paleo, but sometimes we have to do what is necessary to get enough calories.So now I am so scattered trying to figure out how to make things with almond flour without eggs!
Gloria
You never know what you can do until you have to do it.
Tex, Thank you for the long explanation! I really want to truly understand all of this, but there is sooooo much! I am guessing that means I just have to give up coffee. It must be the last thing I have antibodies toward. I am pretty certain all of the others are fine.(all 4 ) Although I do think it is possible that my body makes antibodies to everything I put in it!
Gloria, I am still reeling from her results! My husband was super allergic to milk as a kid, and his mom has cut out gluten. He is gluten free at home, but I suspect he has no desire to give up his burrito every once in a while!
And you are right of course about the calories! I made a pancake yesterday and subbed a banana for the egg. It stuck on the second round, but she liked it. I gather I may have to add in other grains, but I keep reading all of these good reports about healing the gut with the grain free diets! It is hard to ignore, especially for my little ones who have so much ahead of them. At least there is no more refined sugar in our house! Overall they are healthier!
Gloria, I am still reeling from her results! My husband was super allergic to milk as a kid, and his mom has cut out gluten. He is gluten free at home, but I suspect he has no desire to give up his burrito every once in a while!
And you are right of course about the calories! I made a pancake yesterday and subbed a banana for the egg. It stuck on the second round, but she liked it. I gather I may have to add in other grains, but I keep reading all of these good reports about healing the gut with the grain free diets! It is hard to ignore, especially for my little ones who have so much ahead of them. At least there is no more refined sugar in our house! Overall they are healthier!
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So, if your daughter is sensitive to chicken eggs, is it possible to use duck eggs or is that just as bad? Sort of like substituting cow's milk with goat's milk--you still get casein. Do you get similar proteins from both birds and are they so similar that you can't sub one for the other? I suppose that she would develop a sensitivity to the duck eggs given time...?
I am so sorry that this is happening to your family. Its not easy for adults to make the change, but for little kids, it has to be awful. I do not know how you would get anything done except try to protect your kids from well-meaning people who have no clue that what they might offer them could be toxic. Just another example of how screwed up the food industry/our environment when it clashes with genetic make-up.
I am so sorry that this is happening to your family. Its not easy for adults to make the change, but for little kids, it has to be awful. I do not know how you would get anything done except try to protect your kids from well-meaning people who have no clue that what they might offer them could be toxic. Just another example of how screwed up the food industry/our environment when it clashes with genetic make-up.
Jane
Diagnosed with Lymphocytic Colitis 12/19/12
"When it gets dark enough,you can see the stars."
Charles A. Beard
Diagnosed with Lymphocytic Colitis 12/19/12
"When it gets dark enough,you can see the stars."
Charles A. Beard
LE,
Except that I don't condone oral immunotherapy, and I also have reservations about the use of immunotherapy treatment regimens by means of injections. Here's why. Vaccinations work, because they sensitize us to a specific pathogen, so that the next time our immune system discovers that pathogen in our body, it immediately launches an attack against that particular pathogen, and attempts to destroy all replications of it before it can make us sick. IOW, we are able to destroy discrete attacks from that pathogen before they can become a serious threat.
That's not the case with allergens, however, because exposure to most allergens (or intolerances), is not a discrete event — it's typically a chronic event, especially in the case of food allergens. Not only that, but the immune system is incapable of stopping an "attack" by allergens or antigens. The best that it can do is to create inflammation, in hopes of flushing the antigen out of the system. The problem is, this is harder on the body than it is on the allergen.
IOW, this is a totally different problem. Therefore, the theory behind desensitization by immunotherapy methods, is that if we continue to expose the immune system to initially small (too small to provoke much of a response) doses of that antigen, followed by ever-increasing dosages, the immune system is supposed to "learn" to just ignore the antigen. It sounds good in theory, and it appears to be effective, as far as clinical symptoms are concerned, but the problem is that the immune system does not totally ignore that antigen, and in at least certain situations, internal organ damage continues (undetected, in most cases). Here's what I say about it in my book:
24. Burggraf, M., Nakajima-Adachi, H., Hachimura, S., Ilchmann, A., Pemberton, A. D., Kiyono, H., . . . Toda, M. (2011). Oral tolerance induction does not resolve gastrointestinal inflammation in a mouse model of food allergy. Molecular Nutrition & Food Research, 55(10), 1475–1483. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/21714123
Tex
Except that I don't condone oral immunotherapy, and I also have reservations about the use of immunotherapy treatment regimens by means of injections. Here's why. Vaccinations work, because they sensitize us to a specific pathogen, so that the next time our immune system discovers that pathogen in our body, it immediately launches an attack against that particular pathogen, and attempts to destroy all replications of it before it can make us sick. IOW, we are able to destroy discrete attacks from that pathogen before they can become a serious threat.
That's not the case with allergens, however, because exposure to most allergens (or intolerances), is not a discrete event — it's typically a chronic event, especially in the case of food allergens. Not only that, but the immune system is incapable of stopping an "attack" by allergens or antigens. The best that it can do is to create inflammation, in hopes of flushing the antigen out of the system. The problem is, this is harder on the body than it is on the allergen.
IOW, this is a totally different problem. Therefore, the theory behind desensitization by immunotherapy methods, is that if we continue to expose the immune system to initially small (too small to provoke much of a response) doses of that antigen, followed by ever-increasing dosages, the immune system is supposed to "learn" to just ignore the antigen. It sounds good in theory, and it appears to be effective, as far as clinical symptoms are concerned, but the problem is that the immune system does not totally ignore that antigen, and in at least certain situations, internal organ damage continues (undetected, in most cases). Here's what I say about it in my book:
Here's the reference cited in the last paragraph:Let’s explore this issue further, to illustrate how far off track the mainstream medical community has ventured with their treatment of allergies and food sensitivities. Oral immunotheraphy treatments offered by immunolgists are currently in vogue as a way to desensitize patients who have food allergies and food sensitivities. Based on results that show a resolution of clinical symptoms, these treatments are claimed to be very effective in resolving food sensitivities. Immunologists point to the elimination of clinical symptoms and a reduction in IgE antibody levels as proof that their treatments are effective and safe. But do they actually resolve the problem? In my opinion, the answer is a resounding “No!” True, such treatments can eliminate a patient’s clinical symptoms, but as I pointed out in the previous paragraph, antibodies to those allergens continue to be produced in the intestines. This is easily verified by testing for IgA antibody levels by means of appropriate stool tests, or by analyzing biopsy samples taken from the intestines. Serum tests are worthless for this purpose.
Furthermore, researchers have demonstrated that when tolerance to an allergenic food is attained by the use of such desensitizing treatments, damage to the intestines continues to accumulate if the consumption of those foods continues.24 Burggraf et al. (2011) used mice as research subjects to prove that continued feeding brought tolerance (as demonstrated by the resolution of clinical symptoms) and a reduction in IgE antibodies, but inflammation in the jejunum (the middle section of the small intestine) continued to increase. Obviously this raises some serious questions about the validity and safety of the current use of oral immunotheraphy treatments.
24. Burggraf, M., Nakajima-Adachi, H., Hachimura, S., Ilchmann, A., Pemberton, A. D., Kiyono, H., . . . Toda, M. (2011). Oral tolerance induction does not resolve gastrointestinal inflammation in a mouse model of food allergy. Molecular Nutrition & Food Research, 55(10), 1475–1483. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/21714123
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.