Hi Tex. I am wondering what your opinion is of this.... I know that you think that food intolerances are triggered when the MC gene is triggered, right? If that's the case, do you think that all the time that we spent having "IBS" symptoms is because we are already intolerant of certain proteins OR because we already have undiagnosed MC?
Leah
question for Tex about timing of food intolerances
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Hmmmm. You do know how to ask tough questions. That one would probably be suitable for a question on the qualifying exam for a PhD candidate in immunology. 
To be honest, I'm not absolutely certain that the genes that predispose to non-gluten food sensitivities are triggered when the genes that predispose to MC are triggered, (though they certainly might be). I've sort of accepted that theory (for want of a better one) because Dr. Fine maintains that the genes that predispose to gluten sensitivity are triggered when the genes that predispose to MC are triggered. I'm pretty sure that his position on that is correct. But assuming that additional food sensitivities are triggered at the same time may possibly be overly-ambitious, in some cases (and I don't recall that he ever mentioned the possible inclusion of additional food sensitivities).
The reason why I hesitate is because no one really knows why or how these additional food sensitivities develop. Since many/most of them have a molecular structure of one or more of their protein fractions that includes a peptide segment that closely resembles one of the peptides of the gluten molecule that are known antigens, that suggests that the reason for the reactions might possibly be molecular mimicry. If molecular mimicry is involved, then it seems logical that the point in time at which any given reaction threshold is exceeded (thereby triggering a reaction) might well be dependent upon the relative level of sensitivity that is present in the gut.
IOW, the more highly stressed the immune system becomes, the more likely it might be to trigger a reaction against an antigen that is not quite perfect, (that is, not a gluten peptide) but bears a very close resemblance to a known gluten peptide. In this scenario, a non-gluten food sensitivity could develop at any time subsequent to the triggering of one or more of the gluten-sensitive genes. But of course, this theory could be all wet, and it's possible that all sensitivities are triggered at the same time. No one knows the real truth.
But this is irrelevant to your question, anyway, so I apologize for becoming side-tracked so badly.
To answer your question, IMO, the logical sequence of events would suggest that when IBS symptoms first appear, food sensitivities (or drug sensitivities), or some other inflammatory event is already present, but MC is not. Remember that MC is not the cause of the inflammation — MC is actually a symptom — it's a consequence of the inflammation. Some source of enteritis is necessary in order to create the environment where MC can develop. Of course the development of MC is a time-dependent event, so at some point in time enough intestinal damage will have accumulated to meet the criteria for a diagnosis, but prior to that it will not. It's similar to celiac disease in that respect, except that celiac disease takes much longer to generate enough damage to meet the diagnostic criteria.
To look at this from a broader perspective, the chronic inflammation caused by gluten sensitivity, for example, can result in either celiac disease or MC, or both, or it can result in the development of one of the other forms of IBD. MC can develop in any such gluten-initiated event, but celiac disease can only develop if a celiac gene is present. I suspect that Crohn's disease and UC are also associated with certain genes (which are currently unknown). At any rate, this fits my theory that both celiac disease and MC are not actually diseases themselves. Instead, they are symptoms of another disease, namely gluten sensitivity. MC, as it turns out, can also be a symptom of drug-sensitivity. Whether or not celiac disease can also be a symptom of drug-sensitivity, remains to be seen.
To take this up another notch, viewing it from an even broader perspective, with genetics as the controlling factor, a state of chronic inflammation might also result in the development of one or more of any of the other so-called autoimmune diseases (or autoimmune-type diseases, as I prefer to refer to them). IMO, they're autoimmune-type diseases (rather than true autoimmune diseases) because the removal of the exogenous (external) antigen will stop the inflammation and thereby stop the symptoms of the disease.
None of this has been proven by any double-blind, random controlled medical research, of course — it's just my opinion.
Tex
To be honest, I'm not absolutely certain that the genes that predispose to non-gluten food sensitivities are triggered when the genes that predispose to MC are triggered, (though they certainly might be). I've sort of accepted that theory (for want of a better one) because Dr. Fine maintains that the genes that predispose to gluten sensitivity are triggered when the genes that predispose to MC are triggered. I'm pretty sure that his position on that is correct. But assuming that additional food sensitivities are triggered at the same time may possibly be overly-ambitious, in some cases (and I don't recall that he ever mentioned the possible inclusion of additional food sensitivities).
The reason why I hesitate is because no one really knows why or how these additional food sensitivities develop. Since many/most of them have a molecular structure of one or more of their protein fractions that includes a peptide segment that closely resembles one of the peptides of the gluten molecule that are known antigens, that suggests that the reason for the reactions might possibly be molecular mimicry. If molecular mimicry is involved, then it seems logical that the point in time at which any given reaction threshold is exceeded (thereby triggering a reaction) might well be dependent upon the relative level of sensitivity that is present in the gut.
IOW, the more highly stressed the immune system becomes, the more likely it might be to trigger a reaction against an antigen that is not quite perfect, (that is, not a gluten peptide) but bears a very close resemblance to a known gluten peptide. In this scenario, a non-gluten food sensitivity could develop at any time subsequent to the triggering of one or more of the gluten-sensitive genes. But of course, this theory could be all wet, and it's possible that all sensitivities are triggered at the same time. No one knows the real truth.
But this is irrelevant to your question, anyway, so I apologize for becoming side-tracked so badly.
To answer your question, IMO, the logical sequence of events would suggest that when IBS symptoms first appear, food sensitivities (or drug sensitivities), or some other inflammatory event is already present, but MC is not. Remember that MC is not the cause of the inflammation — MC is actually a symptom — it's a consequence of the inflammation. Some source of enteritis is necessary in order to create the environment where MC can develop. Of course the development of MC is a time-dependent event, so at some point in time enough intestinal damage will have accumulated to meet the criteria for a diagnosis, but prior to that it will not. It's similar to celiac disease in that respect, except that celiac disease takes much longer to generate enough damage to meet the diagnostic criteria.
To look at this from a broader perspective, the chronic inflammation caused by gluten sensitivity, for example, can result in either celiac disease or MC, or both, or it can result in the development of one of the other forms of IBD. MC can develop in any such gluten-initiated event, but celiac disease can only develop if a celiac gene is present. I suspect that Crohn's disease and UC are also associated with certain genes (which are currently unknown). At any rate, this fits my theory that both celiac disease and MC are not actually diseases themselves. Instead, they are symptoms of another disease, namely gluten sensitivity. MC, as it turns out, can also be a symptom of drug-sensitivity. Whether or not celiac disease can also be a symptom of drug-sensitivity, remains to be seen.
To take this up another notch, viewing it from an even broader perspective, with genetics as the controlling factor, a state of chronic inflammation might also result in the development of one or more of any of the other so-called autoimmune diseases (or autoimmune-type diseases, as I prefer to refer to them). IMO, they're autoimmune-type diseases (rather than true autoimmune diseases) because the removal of the exogenous (external) antigen will stop the inflammation and thereby stop the symptoms of the disease.
None of this has been proven by any double-blind, random controlled medical research, of course — it's just my opinion.
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 so much for that explanation ....opinion. When I talk to other people about it, it helps to have it straight in my head.
I have one more for you ( if you don't mind). If one is sensitive to soy, does eating it's "relatives" exactly the same as eating soy? What I mean is, does it cause the same inflammation or is it just an irritant? Soy definitely gets me, but green beans do not. So am I doing damage to my gut by eating green beans?
Leah
I have one more for you ( if you don't mind). If one is sensitive to soy, does eating it's "relatives" exactly the same as eating soy? What I mean is, does it cause the same inflammation or is it just an irritant? Soy definitely gets me, but green beans do not. So am I doing damage to my gut by eating green beans?
Leah
Hi Leah,
That's one of the reasons why I feel that molecular mimicry may be a factor in sensitivities of this type. The proteins of every legume each have their own unique molecular structure. That is to say, each of the amino acid chains that define each protein have their own individual arrangement of amino acids in the molecular sequence. If molecular mimicry is involved, then we would expect that some of them might contain amino acid sequences that closely resemble the inflammatory peptides in soy and/or wheat gluten. And conversely, we would expect that some of the legumes would contain proteins that would show a diminished resemblance to those peptides. In fact, they might be so dissimilar that even though we react to soy, and legumes that contain protein fractions that include peptides that closely resemble inflammatory peptides, we might not react at all to the legumes that contain protein fractions that are more dissimilar.
And green beans are a good example of that. Most of us seem to be able to tolerate green beans, even though we might be very sensitive to soy and most legumes. Of course, that doesn't apply to everyone, because some people have problems with green beans, also.
The question about damage is not so easy. I'm inclined to believe that damage is probably not involved in that particular situation. In the scenario where we initially react to a food, and then develop a tolerance for it, it's a different situation. Research on rodents shows that in an induced-tolerance situation, antibodies are still being produced, and if antibodies are being produced, then damage continues to acrue, even in the absence of clinical symptoms.
So if we never show a sensitivity to a food, then we are probably home free. If we initially react to it, and subsequently develop a tolerance, then we are probably continuing to accrue damage. IOW, there's no simple yes or no answer in all cases.
At least that's how I see it, FWIW.
Tex
That's one of the reasons why I feel that molecular mimicry may be a factor in sensitivities of this type. The proteins of every legume each have their own unique molecular structure. That is to say, each of the amino acid chains that define each protein have their own individual arrangement of amino acids in the molecular sequence. If molecular mimicry is involved, then we would expect that some of them might contain amino acid sequences that closely resemble the inflammatory peptides in soy and/or wheat gluten. And conversely, we would expect that some of the legumes would contain proteins that would show a diminished resemblance to those peptides. In fact, they might be so dissimilar that even though we react to soy, and legumes that contain protein fractions that include peptides that closely resemble inflammatory peptides, we might not react at all to the legumes that contain protein fractions that are more dissimilar.
And green beans are a good example of that. Most of us seem to be able to tolerate green beans, even though we might be very sensitive to soy and most legumes. Of course, that doesn't apply to everyone, because some people have problems with green beans, also.
The question about damage is not so easy. I'm inclined to believe that damage is probably not involved in that particular situation. In the scenario where we initially react to a food, and then develop a tolerance for it, it's a different situation. Research on rodents shows that in an induced-tolerance situation, antibodies are still being produced, and if antibodies are being produced, then damage continues to acrue, even in the absence of clinical symptoms.
So if we never show a sensitivity to a food, then we are probably home free. If we initially react to it, and subsequently develop a tolerance, then we are probably continuing to accrue damage. IOW, there's no simple yes or no answer in all cases.
At least that's how I see it, FWIW.
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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wmonique2
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question for Tex...
Following up on Leah's questions---if one tests positive for soy sensitivity (while being asymptomatic), does that mean that it is wise to stay away from all legumes?
Thanks, Tex.
Monique
Thanks, Tex.
Monique
Diagnosed 2011 with LC. Currently on Low Dose Naltrexone (LDN)
Probably, if it was a definitive test result — that is, if it was at least 12 or higher. If the result was a 10 or 11, there's a small statistical chance that it might have been a false positive test result, because a few of the low positive scores will fall into that category.
A lot of people in the general population probably wouldn't have the will power to do that, without clinical symptoms, but most members of this board seem to have above-average willpower.
Tex
A lot of people in the general population probably wouldn't have the will power to do that, without clinical symptoms, but most members of this board seem to have above-average willpower.
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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Sheila
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Hey Tex, I think members of this Board have higher than usual willpower because we know exactly what the consequences will be if we go off our diet. I'm sure all of us have an awful memory of the worst day (or night) before being diagnosed, the worst "accident", the embarrassment of stomach rumbles and room-clearing gas. This also seems to be a pretty smart group. I wonder if there is any correlation between I.Q. and the incidence of MC/celiac.
Sheila W[/i]
Sheila W[/i]
To get something you never had, you have to do something you never did.
A person who never made a mistake never tried something new. Einstein
A person who never made a mistake never tried something new. Einstein
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I agree with you Sheila. I'm not even sure I would call it willpower. It's more fear of being so sick that I live my life in the bathroom. I can't think of a single food that is worth it.Sheila wrote:Hey Tex, I think members of this Board have higher than usual willpower because we know exactly what the consequences will be if we go off our diet. I'm sure all of us have an awful memory of the worst day (or night) before being diagnosed, the worst "accident", the embarrassment of stomach rumbles and room-clearing gas. This also seems to be a pretty smart group. I wonder if there is any correlation between I.Q. and the incidence of MC/celiac.
Sheila W[/i]
Jean
Sheila,
I'm sure you're right about the motivation. The disease tends to create some pretty convincing incentives. Even so, I find it relatively easy to avoid dairy products, based on a positive antibody test result, even though they cause no noticeable clinical symptoms for me.
And as you pointed out, there probably exists an association between IQ and a predisposition to MC/celiac disease, because it's clear that a high percentage of us are inclined to be perfectionists, early adapters, innovators, etc., and/or a type A personality.
Tex
I'm sure you're right about the motivation. The disease tends to create some pretty convincing incentives. Even so, I find it relatively easy to avoid dairy products, based on a positive antibody test result, even though they cause no noticeable clinical symptoms for me.
And as you pointed out, there probably exists an association between IQ and a predisposition to MC/celiac disease, because it's clear that a high percentage of us are inclined to be perfectionists, early adapters, innovators, etc., and/or a type A personality.
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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wmonique2
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I agree.tex wrote:Sheila,
And as you pointed out, there probably exists an association between IQ and a predisposition to MC/celiac disease, because it's clear that a high percentage of us are inclined to be perfectionists, early adapters, innovators, etc., and/or a type A personality.
Tex
Monique
Diagnosed 2011 with LC. Currently on Low Dose Naltrexone (LDN)
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Carriagehouse
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I agree, too! And in my case, also a determination to prove all the close-minded GI's wrong ~ when mine said with a half smile, "Good luck trying to control symptoms with diet changes, call me when you're ready for the meds," that was the challenge I needed to prove him wrong. Tell me I can't do something and it's all the motivation I need ;)
Leslie
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Diagnosed with Lymphocytic Colitis on December 5, 2012
True friendship is like sound health ... the value is seldom appreciated until it is lost ~ Charles Caleb Colton
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Diagnosed with Lymphocytic Colitis on December 5, 2012
True friendship is like sound health ... the value is seldom appreciated until it is lost ~ Charles Caleb Colton
I'm another that agrees with this...I'm definitely a high, overachiever, Type A personality type.tex wrote:Sheila,
And as you pointed out, there probably exists an association between IQ and a predisposition to MC/celiac disease, because it's clear that a high percentage of us are inclined to be perfectionists, early adapters, innovators, etc., and/or a type A personality.
Tex
As things that you just don't do, go, that ranks right up there with, "You don't spit into the wind", and "You don't tug on Superman's cape".Leslie wrote:when mine said with a half smile, "Good luck trying to control symptoms with diet changes, call me when you're ready for the meds," that was the challenge I needed to prove him wrong.
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.
