Tex,
Here are 2 research articles that found antibodies to the gut bacteria. (Red emphasis mine).
1.) Clin Dev Immunol. 2004 Sep-Dec;11(3-4):195-204.
Inflammatory bowel disease: autoimmune or immune-mediated pathogenesis?Wen Z, Fiocchi C.
SourceDivision of Gastroenterology, University Hospitals of Cleveland, Case Western Reserve University School of Medicine, Cleveland, OH 44106-4952, USA.
Abstract
The pathogenesis of Crohn's disease (CD) and ulcerative colitis (UC), the two main forms of inflammatory bowel disease (IBD), is still unclear, but both autoimmune and immune-mediated phenomena are involved. Autoimmune phenomena include the presence of serum and mucosal autoantibodies against intestinal epithelial cells in either form of IBD, and against human tropomyosin fraction five selectively in UC. In addition, perinuclear antineutrophil cytoplasmic antibodies (pANCA) are common in UC, whereas antibodies against Saccharomyces cerevisiae (ASCA) are frequently found in CD. Immune-mediate phenomena include a variety of abnormalities of humoral and cell-mediated immunity, and a generalized enhanced reactivity against intestinal bacterial antigens in both CD and UC. It is currently believed that loss of tolerance against the indigenous enteric flora is the central event in IBD pathogenesis. Various complementary factors probably contribute to the loss of tolerance to commensal bacteria in IBD. They include defects in regulatory T-cell function, excessive stimulation of mucosal dendritic cells, infections or variants of proteins critically involved in bacterial antigen recognition, such as the products of CD-associated NOD2/CARD15 mutations.
2.)antibodies in inflammatory bowel disease are directed against intestinal bacteria.
A Macpherson, U Y Khoo, I Forgacs, J Philpott-Howard, and I Bjarnason
Department of Medicine, King's College School of Medicine, London.
Abstract
In contrast with normal subjects where IgA is the main immunoglobulin in the intestine, patients with active inflammatory bowel disease (IBD) produce high concentrations of IgG from intestinal lymphocytes, but the antigens at which these antibodies are directed are unknown. To investigate the specificities of these antibodies mucosal immunoglobulins were isolated from washings taken at endoscopy from 21 control patients with irritable bowel syndrome, 10 control patients with intestinal inflammation due to infection or ischaemia, and 51 patients with IBD: 24 Crohn's disease (CD, 15 active, nine quiescent), 27 ulcerative colitis (UC, 20 active, seven inactive). Total mucosal IgG was much higher (p < 0.001) in active UC (median 512 micrograms/ml) and active CD (256 micrograms/ml) than in irritable bowel syndrome controls (1.43 micrograms/ml), but not significantly different from controls with non-IBD intestinal inflammation (224 micrograms/ml). Mucosal IgG bound to proteins of a range of non-pathogenic commensal faecal bacteria in active CD; this was higher than in UC (p < 0.01); and both were significantly greater than controls with non-IBD intestinal inflammation (CD p < 0.001, UC p < 0.01) or IBS (p < 0.001 CD and UC). This mucosal IgG binding was shown on western blots and by enzyme linked immunosorbent assay (ELISA) to be principally directed against the bacterial cytoplasmic rather than the membrane proteins. Total mucosal IgA concentrations did not differ between IBD and controls, but the IgA titres against faecal bacteria were lower in UC than controls (p < 0.01). These experiments show that there is an exaggerated mucosal immune response particularly in active CD but also in UC directed against cytoplasmic proteins of bacteria within the intestinal lumen; this implies that in relapse of IBD there is a breakdown of tolerance to the normal commensal flora of the gut.
Actually, I'll try to contact Dr. Fine and see if I can get his current thinking on this.
Love,
Polly
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Hi Polly,
Thanks for the references. The problem with all of the research on this topic is that the authors keep repeating the same theory, but they never prove anything — the evidence is all circumstancial. No one knows whether these antibodies against gut bacteria actually play a part in the etiology of IBD, or whether they are a consequence (symptom) of IBD. No research evidence exists to distinguish which concept is the correct one. IOW, the presence of antibodies against gut bacteria may well be a natural consequence of the disease (rather than a cause). After all, look at this statement from the last quote that you listed:
Anyway, to go even further, the last half of the sentence that I re-quoted claims that lower antibody levels against gut bacteria exist in UC patients, than in controls. What? That obviously appears to contradict the claims that gut bacteria play a part in the etiology of UC — UNLESS, we assume that the controls were in the early stages of developing an IBD (which, IMO, was probably the case, since the controls had either "IBS" or "intestinal inflammation due to infection or ischaemia"). IOW, IMO these researchers confounded their research results by not recognizing that "IBS" and "intestinal inflammation due to infection or ischaemia" are very likely to be either predisposing conditions for IBD, or early stages of IBD. If that were the case, then it would not necessarily be so surprising that the antibody level (against gut bacteria) might be lower in UC patients, after the disease has matured.
All in all, though, I don't see any compelling evidence that immune system reactions against gut bacteria are a primary cause of IBDs. The evidence found in currently available research data merely shows that the phenomenon is associated with IBDs. Whether it is associated with the etiology of IBDs, or it is a result of IBDs, remains to be seen.
If a majority of GI specialists are going to claim that diet has no effect on MC (because no random, double-blind test has been done to prove the concept), then I am certainly going to deny the validity of their feeble claim that antibodies against gut bacteria are a primary cause of IBD, until they come up with some truly convincing evidence that what they say is true. This is a two-way street.
Consider this: We know (by Dr. Fine's research) that when the genes that predispose to MC are actually triggered, the genes that predispose to certain food sensitivities are also triggered. This in itself is going to change the gut bacteria balance drastically, due to the poorly digested food, and the eventual diet changes. Note that this is a consequence of the disease, though, not a cause. It wouldn't be much of a stretch of the imagination to visualize the possibility that when all these other genes are triggered, perhaps certain genes that predispose to a loss of tolerance for certain gut bacteria are also triggered. This would certainly explain how our immune system might suddenly begin to fail to recognize certain gut bacteria as "self", and launch a campaign to attempt to eradicate them. Again, though, this would be a result of the development of MC (or another IBD), not a cause.
In the meantime, I maintain that chronic stress creates the "perfect" environment that initiates the development of IBDs. Everything else is secondary, or consequential.
Love,
Tex
Thanks for the references. The problem with all of the research on this topic is that the authors keep repeating the same theory, but they never prove anything — the evidence is all circumstancial. No one knows whether these antibodies against gut bacteria actually play a part in the etiology of IBD, or whether they are a consequence (symptom) of IBD. No research evidence exists to distinguish which concept is the correct one. IOW, the presence of antibodies against gut bacteria may well be a natural consequence of the disease (rather than a cause). After all, look at this statement from the last quote that you listed:
That's a rather profound finding, if you ask me. The first half of the sentence says that the acute (mucosal) inflammation levels were no different between IBD patients and controls. When I first saw that statement, I thought that it obviously conflicts with Dr. Fine's decision to use IgA antibodies for his testing procedures, because it claims that his entire concept for testing is invalid. Remember that IgA antibodies are what Dr. Fine uses in his ELISA stool testing, because they indicate current responses to antigens, where IgG antibodies are a result of long-term reactions. But then it dawned on me that the controls in this research project also had compromised digestive systems. Dr. Fine wasn't concerned about the distinction between "IBS" and IBDs — he was only interested in food sensitivities, and obviously, people who have "IBS" also have food sensitivities. This second reference was published in 1996, which was during roughly the same time frame when Dr. Fine was doing most of his research.Total mucosal IgA concentrations did not differ between IBD and controls, but the IgA titres against faecal bacteria were lower in UC than controls (p < 0.01).
Anyway, to go even further, the last half of the sentence that I re-quoted claims that lower antibody levels against gut bacteria exist in UC patients, than in controls. What? That obviously appears to contradict the claims that gut bacteria play a part in the etiology of UC — UNLESS, we assume that the controls were in the early stages of developing an IBD (which, IMO, was probably the case, since the controls had either "IBS" or "intestinal inflammation due to infection or ischaemia"). IOW, IMO these researchers confounded their research results by not recognizing that "IBS" and "intestinal inflammation due to infection or ischaemia" are very likely to be either predisposing conditions for IBD, or early stages of IBD. If that were the case, then it would not necessarily be so surprising that the antibody level (against gut bacteria) might be lower in UC patients, after the disease has matured.
All in all, though, I don't see any compelling evidence that immune system reactions against gut bacteria are a primary cause of IBDs. The evidence found in currently available research data merely shows that the phenomenon is associated with IBDs. Whether it is associated with the etiology of IBDs, or it is a result of IBDs, remains to be seen.
If a majority of GI specialists are going to claim that diet has no effect on MC (because no random, double-blind test has been done to prove the concept), then I am certainly going to deny the validity of their feeble claim that antibodies against gut bacteria are a primary cause of IBD, until they come up with some truly convincing evidence that what they say is true. This is a two-way street.
Consider this: We know (by Dr. Fine's research) that when the genes that predispose to MC are actually triggered, the genes that predispose to certain food sensitivities are also triggered. This in itself is going to change the gut bacteria balance drastically, due to the poorly digested food, and the eventual diet changes. Note that this is a consequence of the disease, though, not a cause. It wouldn't be much of a stretch of the imagination to visualize the possibility that when all these other genes are triggered, perhaps certain genes that predispose to a loss of tolerance for certain gut bacteria are also triggered. This would certainly explain how our immune system might suddenly begin to fail to recognize certain gut bacteria as "self", and launch a campaign to attempt to eradicate them. Again, though, this would be a result of the development of MC (or another IBD), not a cause.
In the meantime, I maintain that chronic stress creates the "perfect" environment that initiates the development of IBDs. Everything else is secondary, or consequential.
Love,
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.
Here's more evidence that researchers continue to be pretty much confused about the issue of gut bacteria. Here's a quote from a very recently-published article:
Researchers could learn a lot from buzzards. Buzzards often become quite numerous around road kills and other carcasses. But that doesn't mean that the buzzards had anything to do with the cause of death. Researchers need to learn to look at the early stages of disease development, rather than studying the circumstantial evidence after the fact, and then trying to make assumptions about the chain of events that led up to that point. Forensic studies sometimes leave a lot to be desired.
Tex
http://www.netdoctor.co.uk/interactive/ ... -t116.htmlA bacterium originally thought to play a protective role in the gut may in fact be involved in the development of Crohn's disease, scientists say.
Faecalibacterium prausnitzii has anti-inflammatory properties and was therefore thought to help protect against the bowel disorder.
But a new study in the American Journal of Gastroenterology has uncovered significantly elevated levels of the bacterium in the bowels of children with Crohn's disease, prompting the researchers to view it in a different light.
Researchers could learn a lot from buzzards. Buzzards often become quite numerous around road kills and other carcasses. But that doesn't mean that the buzzards had anything to do with the cause of death. Researchers need to learn to look at the early stages of disease development, rather than studying the circumstantial evidence after the fact, and then trying to make assumptions about the chain of events that led up to that point. Forensic studies sometimes leave a lot to be desired.
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.
Dr. Mercola weighed in on this debate today. The research is very compelling:
http://articles.mercola.com/sites/artic ... _DNL_art_1Recent research published in the journal Science may shed much needed light on the persistent and hard-to-treat nature of irritable bowel disease (IBD). The researchers infected mice with Toxoplasma gondii, a parasite associated with lethal food-borne illness.
Interestingly, when the immune system of the mouse reacted to the presence of the parasite, it also began overreacting to beneficial bacteria. In fact, while about 10 percent of the T cells in the GI tract attacked the parasite, approximately 45 percent of the T cells began attacking other gut microbes. Furthermore, once the parasite had been successfully cleared, the immune system continued to misidentify beneficial bacteria as a foreign agents, preventing the mice from ever fully recovering from the infection. As stated by Time:
"If something similar happens in humans – either with Toxoplasma gondii or another invader – it could go a long way to explaining both the existence and persistence of all of the IBD conditions."
According to the National Institute of Allergy and Infectious Diseases:
"The team's findings are among the first to demonstrate that T cells in the gut mount an immune response to commensal bacteria [normal microflora] during an infection. They also are the first to show that commensal-specific T cells remain in circulation after the infection is cleared. Based on their observations, the investigators speculate that, when uncontrolled, commensal-specific T cells may contribute to development of Crohn's disease, but more research is needed."
Zizzle,
That appears to be very convincing evidence. However, if that is true, then how do we explain why so many of us have managed to achieve remission, and continue to maintain it, simply by eliminating food sensitivities from our diet? It's hard to argue with success, despite research claims to the contrary.
IOW, while I find that research to be very illuminating, I'm still not convinced that loss of tolerance of commensal gut bacteria is the cause of MC, because that obviously flies in the face of our own personal experiences. It would be impossible for us to be in remission if that theory were true.
Celiac disease is also an IBD. If loss of tolerance of commensal gut bacteria causes celiac disease, then why does simply avoiding gluten bring remission (for many/most, at least)? The only way that could be true is if the only gut bacteria that the rogue T cells attack, are the ones that can only survive in the presence of gluten in the diet. That seems extremely unlikely, if not impossible.
FWIW, they have proven that the theory is possible. But we had already assumed that it was possible, a decade or two ago. So really this is not exactly earth-shaking information, because it provides no evidence that this phenomenon actually causes IBD in vivo. One can do amazing things in a laboratory setting, but that doesn't necessarily prove that it will happen in real life, by natural processes.
That said, I certainly haven't written it off as a possibility in the etiology of IBD, I'm just saying that I doubt that it's a primary cause.
Tex
That appears to be very convincing evidence. However, if that is true, then how do we explain why so many of us have managed to achieve remission, and continue to maintain it, simply by eliminating food sensitivities from our diet? It's hard to argue with success, despite research claims to the contrary.
IOW, while I find that research to be very illuminating, I'm still not convinced that loss of tolerance of commensal gut bacteria is the cause of MC, because that obviously flies in the face of our own personal experiences. It would be impossible for us to be in remission if that theory were true.
Celiac disease is also an IBD. If loss of tolerance of commensal gut bacteria causes celiac disease, then why does simply avoiding gluten bring remission (for many/most, at least)? The only way that could be true is if the only gut bacteria that the rogue T cells attack, are the ones that can only survive in the presence of gluten in the diet. That seems extremely unlikely, if not impossible.
FWIW, they have proven that the theory is possible. But we had already assumed that it was possible, a decade or two ago. So really this is not exactly earth-shaking information, because it provides no evidence that this phenomenon actually causes IBD in vivo. One can do amazing things in a laboratory setting, but that doesn't necessarily prove that it will happen in real life, by natural processes.
That said, I certainly haven't written it off as a possibility in the etiology of IBD, I'm just saying that I doubt that it's a primary cause.
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.
This is all very interesting. Being a Celiac, I get Facebook posts from the University of Chicago's Celiac research team. Of course, they are working on a cure. One of their posts stated that 40-60% ( may be off on the numbers slightly) of Celiac patients are not getting better on a 100% GF diet. Being a Celiac, this is very discouraging to me. They didn't comment on Dr. Osborne's commentary that perhaps Celiacs are also reacting to the gluten in what are considered our safe grains. Especially, corn, which has high storage proteins in it.
Also, couldn't it be possible that Celiacs aren't getting better because they are eating GF processed foods, that always contain traces of gluten in them? And the more you eat them, the more traces of Gluten you're ingesting? Is the Quinoa/corn GF pasta I'm eating contain some gluten in it? Does my Rice Chex have traces of gluten? Just a note to myself that I may need to give up ALL processed foods.
The possibility of our bodies attacking our own bacteria is very disturbing. And I still wonder often how a lot of people are not able to reach remission even after giving up all reactive foods.
A part deep inside of me thinks that with IBD's, it may not be ALL about the diet after all. Just wish they could come up with a cure for them. IBD's are just such miserable diseases.
Terri
Also, couldn't it be possible that Celiacs aren't getting better because they are eating GF processed foods, that always contain traces of gluten in them? And the more you eat them, the more traces of Gluten you're ingesting? Is the Quinoa/corn GF pasta I'm eating contain some gluten in it? Does my Rice Chex have traces of gluten? Just a note to myself that I may need to give up ALL processed foods.
The possibility of our bodies attacking our own bacteria is very disturbing. And I still wonder often how a lot of people are not able to reach remission even after giving up all reactive foods.
A part deep inside of me thinks that with IBD's, it may not be ALL about the diet after all. Just wish they could come up with a cure for them. IBD's are just such miserable diseases.
Terri
Diagnosed with Lymphocytic Colitis in July, 2012 then with Celiac in November, 2012.
I suspect that you are right on target. Cross-contamination is ubiquitous, and IMO, anyone who is sensitive to gluten is much more sensitive than the "experts" give them credit for. Just because we do not show clinical symptoms, does not mean that we are not ingesting enough gluten in our diet to be right on the verge of reacting at any time.Terri wrote:Also, couldn't it be possible that Celiacs aren't getting better because they are eating GF processed foods, that always contain traces of gluten in them? And the more you eat them, the more traces of Gluten you're ingesting?
How can anyone know for certain that they have removed "all reactive foods" from their diet?And I still wonder often how a lot of people are not able to reach remission even after giving up all reactive foods.
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.
Just wish that U of C would answer most people's questions. Their vague posts leave most of us hanging and often questions do not get answered. When I mentioned possible other food intolerances, they basically said (in their own confusing language) that that wasn't the issue and they pretty much diced Enterolabs and their testing. They know a lot more than what they are saying!
Some people on this board seem to react to everything and this saddens me as this disease becomes more confusing and depressing by the minute. Just how many of us have actually gone into remission anyway and no longer having symptoms? Is it a high percentage? So frustrating as I know a lot of people from the past no longer post and so we have no way of knowing. Knowing that there are success stories out there gives me hope!
Sorry, but a little down today and I have no reason to be because I feel great. I just feel so bad for the people who aren't feeling better even after giving up so many foods (even for years) and sometimes I think my days are numbered and the mighty beast will wake up once again. I will try to remain positive. Just one of those days!
Terri
Some people on this board seem to react to everything and this saddens me as this disease becomes more confusing and depressing by the minute. Just how many of us have actually gone into remission anyway and no longer having symptoms? Is it a high percentage? So frustrating as I know a lot of people from the past no longer post and so we have no way of knowing. Knowing that there are success stories out there gives me hope!
Sorry, but a little down today and I have no reason to be because I feel great. I just feel so bad for the people who aren't feeling better even after giving up so many foods (even for years) and sometimes I think my days are numbered and the mighty beast will wake up once again. I will try to remain positive. Just one of those days!
Terri
Diagnosed with Lymphocytic Colitis in July, 2012 then with Celiac in November, 2012.
Or they know a lot less than what they are saying.Terri wrote:They know a lot more than what they are saying!
Just how many of us have actually gone into remission anyway and no longer having symptoms? Is it a high percentage? So frustrating as I know a lot of people from the past no longer post and so we have no way of knowing. Knowing that there are success stories out there gives me hope!
A very high percentage — far, far higher than the GI medical community is able to achieve, because when they decide to stop prescribing a corticosteroid for their patients, the vast majority of them relapse within a few weeks.
Most people stop posting for one of two reasons:
1. They are unable to muster the self-control needed to follow a rigid diet, so they choose to live with the symptoms.
2. They stop posting because their symptoms are resolved (or vastly improved), so they no longer feel any need to hang out here.
This is a very complex disease, and we are all different in our symptoms, and how we react to treatment.
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.
Terri,
But I also suspect that my case has taken so long to resolve because I was eating flours that were contaminated, perhaps ever so slightly, with gluten. It never occurred to me that corn flour I was using could be contaminated until this past spring. I had given up rice flour the year before, and replaced it with corn flour - from the same company, SWAD, a company that makes many Indian products and flours. I noticed that the corn tortillas I was making suddenly held together a little better. I suspected gluten contamination. My MC symptoms began to get worse around the same time. I stopped using their corn flour and began grinding my own, using whole corn kernels. I began getting better and have been seeing Normans most of the time since. I've also been able to reduce the Entocort I'm taking.
I've begun to realize that prior to using SWAD'S corn flour, I used their rice flour. It seems reasonable to me that the rice flour could have been slightly contaminated just as the corn flour likely was. I used their rice flour for at least 3 years. I could have ground it, but it was just as cheap to buy it already ground. The company made no claims that either flour was gluten-free. I assumed it was. It's very easy for products to be contaminated with flours from previous runs if the company doesn't take care to scrupulously clean the equipment or use dedicated equipment.
I will only buy corn flour now that states that it is gluten-free, or I will grind the grain myself. I recently bought corn meal which didn't say it was gluten-free, but it did say it was free of allergens, so I'm hoping I'm safe. I grind it into flour. So far, I'm continuing to do well while using it.
I've been on the board for enough years to know that many people have gotten better by following the advice given here. That's why I'm still here; I have faith in the process. The human tendency is to move on after getting over a crisis. Most people here follow that pattern after getting better, but a few stay and help lift up others. I'm ever grateful for them. They deserve a special place in Heaven.
Gloria
I suspect you may be referring to me, and that saddens me! I'm not a typical member of the board; quite the opposite. I have a couple of issues affecting me: Double DQ1 genes and mast cell issues.Terri wrote:Some people on this board seem to react to everything and this saddens me as this disease becomes more confusing
But I also suspect that my case has taken so long to resolve because I was eating flours that were contaminated, perhaps ever so slightly, with gluten. It never occurred to me that corn flour I was using could be contaminated until this past spring. I had given up rice flour the year before, and replaced it with corn flour - from the same company, SWAD, a company that makes many Indian products and flours. I noticed that the corn tortillas I was making suddenly held together a little better. I suspected gluten contamination. My MC symptoms began to get worse around the same time. I stopped using their corn flour and began grinding my own, using whole corn kernels. I began getting better and have been seeing Normans most of the time since. I've also been able to reduce the Entocort I'm taking.
I've begun to realize that prior to using SWAD'S corn flour, I used their rice flour. It seems reasonable to me that the rice flour could have been slightly contaminated just as the corn flour likely was. I used their rice flour for at least 3 years. I could have ground it, but it was just as cheap to buy it already ground. The company made no claims that either flour was gluten-free. I assumed it was. It's very easy for products to be contaminated with flours from previous runs if the company doesn't take care to scrupulously clean the equipment or use dedicated equipment.
I will only buy corn flour now that states that it is gluten-free, or I will grind the grain myself. I recently bought corn meal which didn't say it was gluten-free, but it did say it was free of allergens, so I'm hoping I'm safe. I grind it into flour. So far, I'm continuing to do well while using it.
I've been on the board for enough years to know that many people have gotten better by following the advice given here. That's why I'm still here; I have faith in the process. The human tendency is to move on after getting over a crisis. Most people here follow that pattern after getting better, but a few stay and help lift up others. I'm ever grateful for them. They deserve a special place in Heaven.
Gloria
You never know what you can do until you have to do it.
OH Gloria, you are one very tough lady....so much perseverance. How do you do it? I've never thought about corn and rice flours being contaminated. Yikes! I would assume those flours were gluten free as well. This contamination thing really stinks!
Hope you are able to get off Entocort one day. Sounds like you are doing well and that's what I need to hear right now. I haven't been on the board long enough to know everyone's stories. I still have lots to read on this forum! Still trying to understand this mast cell stuff but hoping I don't have that problem. I eat some high histamine foods and don't seem to react to them just yet. It was the beta blockers that set me off which makes me think maybe I do have some mast cell issue but don't really know for sure.
So thankful also for the people on this forum who stick around to help us newbies out (yep I still consider myself a newbie) and also to help out those who seem to still be struggling.
And as I recall if it weren't for you, I would have never known that generic Imodium had lactose in it!
Terri
Hope you are able to get off Entocort one day. Sounds like you are doing well and that's what I need to hear right now. I haven't been on the board long enough to know everyone's stories. I still have lots to read on this forum! Still trying to understand this mast cell stuff but hoping I don't have that problem. I eat some high histamine foods and don't seem to react to them just yet. It was the beta blockers that set me off which makes me think maybe I do have some mast cell issue but don't really know for sure.
So thankful also for the people on this forum who stick around to help us newbies out (yep I still consider myself a newbie) and also to help out those who seem to still be struggling.
And as I recall if it weren't for you, I would have never known that generic Imodium had lactose in it!
Terri
Diagnosed with Lymphocytic Colitis in July, 2012 then with Celiac in November, 2012.
Gloria:
I wonder about it with my 6 year old grandson. His mother and many in her family have Celiac Disease . She has a gluten-free house, and all 3 kids have been gluten-free since the day they were born. My grandson is extremely sensitive to gluten, much more so than the other 2 grandkids. Just the presence of flour dust in the air gives him a bad rash on his face and scalp. Any slip-up and he has a major reaction with diarrhea for several days. And he is tiny for his age, and quite skinny. So I can't help but wonder if cross-contamination is giving him enough gluten to affect his gut and cause some malabsorbtion issues. I would be very curious to see what an Enterolab test might show for anti-gluten antibodies. Since he has been gluten-free for life, except for a very few accidental exposures, I would assume that a significant antibody level would indicate cross-contamination. I recall that Tex got tested after many years of being gluten free and had a fairly high antibody level.
Of course that begs the question as to what to do next for those of us who suspect cross-contamination. It's a very daunting prospect, given the present state of agriculture and food processing. I guess we each have to figure out how careful we need to be in order to keep symptoms at a manageable level for us. It's never easy.......
Rosie
I, too, wonder if the time it takes for us to heal is lengthened by the often unrecognized cross-contamination. We all differ in sensitivity, and for some, like you, it can be a major stumbling block.But I also suspect that my case has taken so long to resolve because I was eating flours that were contaminated, perhaps ever so slightly, with gluten. It never occurred to me that corn flour I was using could be contaminated until this past spring. I had given up rice flour the year before, and replaced it with corn flour - from the same company, SWAD, a company that makes many Indian products and flours. I noticed that the corn tortillas I was making suddenly held together a little better. I suspected gluten contamination. My MC symptoms began to get worse around the same time. I stopped using their corn flour and began grinding my own, using whole corn kernels. I began getting better and have been seeing Normans most of the time since. I've also been able to reduce the Entocort I'm taking.
I wonder about it with my 6 year old grandson. His mother and many in her family have Celiac Disease . She has a gluten-free house, and all 3 kids have been gluten-free since the day they were born. My grandson is extremely sensitive to gluten, much more so than the other 2 grandkids. Just the presence of flour dust in the air gives him a bad rash on his face and scalp. Any slip-up and he has a major reaction with diarrhea for several days. And he is tiny for his age, and quite skinny. So I can't help but wonder if cross-contamination is giving him enough gluten to affect his gut and cause some malabsorbtion issues. I would be very curious to see what an Enterolab test might show for anti-gluten antibodies. Since he has been gluten-free for life, except for a very few accidental exposures, I would assume that a significant antibody level would indicate cross-contamination. I recall that Tex got tested after many years of being gluten free and had a fairly high antibody level.
Of course that begs the question as to what to do next for those of us who suspect cross-contamination. It's a very daunting prospect, given the present state of agriculture and food processing. I guess we each have to figure out how careful we need to be in order to keep symptoms at a manageable level for us. It's never easy.......
Rosie
Our greatest weakness lies in giving up. The most certain way to succeed is always to try just one more time………Thomas Edison
Hi Terri,
Long term remission is quite possible. Heck, my last colonoscopy result found that the number of lymphocytes was low enough that I don't even meet the diagnostic criteria anymore. I have avoided gluten and dairy for ages - it was always dairy that gave me D and gluten gives me swellings, joint pain fog etc.. I do still get the odd soft BM, but frankly I think that is fairly normal. Especially if I have eaten cashews or overdone other nuts
I know I get glutened by contamination too regularly. I guess I also pay more attention to bowel habits than the average person. 
I don't post here very often these days, but I still drop by and read regularly.
My new years resolution was to lose weight by using a closer to paleo diet. I know it suits my body, but I have let some really bad junk food habits get the upper hand. In a way it is helpful that the weight has crept up way too far, as hubby can see the need to do something and is actually trying (in his own way) to help.
Anyway, take heart. You can get your life back, no doubt about it. The path just varies and sometimes it can be tricky to find YOUR path.
Lyn
Long term remission is quite possible. Heck, my last colonoscopy result found that the number of lymphocytes was low enough that I don't even meet the diagnostic criteria anymore. I have avoided gluten and dairy for ages - it was always dairy that gave me D and gluten gives me swellings, joint pain fog etc.. I do still get the odd soft BM, but frankly I think that is fairly normal. Especially if I have eaten cashews or overdone other nuts
I know I get glutened by contamination too regularly. I guess I also pay more attention to bowel habits than the average person. I don't post here very often these days, but I still drop by and read regularly.
My new years resolution was to lose weight by using a closer to paleo diet. I know it suits my body, but I have let some really bad junk food habits get the upper hand. In a way it is helpful that the weight has crept up way too far, as hubby can see the need to do something and is actually trying (in his own way) to help.
Anyway, take heart. You can get your life back, no doubt about it. The path just varies and sometimes it can be tricky to find YOUR path.
Lyn