Hiya Tex,
Here is something I have been wondering about.....you said you had a flare recently because of kidney stones. Since you no longer have a colon, you can therefore no longer have microscopic COLitis, since that, by definition means inflammation in the COLon. (Of course, we know that inflammation can occur anywhere in the GI tract when one has MC, so are you referring to a flare caused by enteritis - small bowel inflammation?). Or generalized symptoms like brain fog, arthritis, fatigue? Just curious about what you see as the mechanism for the flare.
Love,
Polly
Question for Tex
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Question for Tex
Blessed are they who can laugh at themselves, for they shall never cease to be amused.
Hi Polly,
That's a very good question. And of course my first point is that MC is improperly named and/or improperly described in the medical literature, because there are volumes of research data that clearly show that the disease can affect not only both the large and small bowel, but other parts of the digestive tract as well. But in the example you noted, I did indeed have inflammation of the colon, as you will see below. I hope that I can explain my line of reasoning in a way that makes sense, because I should already be in bed, so I may accidentally leave out some important points, but here goes:
As you are aware, there are a few old medical articles that conclude that diversion of the fecal stream (by means of an ileostomy) cures MC. I have long maintained that those articles are bogus. Remember the lady who joined us roughly 4 or 5 years ago, who was persuaded by her doctors to agree to an ileostomy as a treatment for her MC that was refractive to treatment by other means? We tried in vain to persuade her not to agree to the procedure, but she went ahead anyway. And sadly, just as we feared, the procedure made no difference. She continued to react.
Since I have an ileostomy, it is rather easy for me to verify that the claims in those old articles don't hold up to even the simplest of tests. If I eat any of the triggers that caused me to react prior to my resection procedure, I still react with D (through the stoma), so this supports our contention that MC can affect either the large or small bowel.
Remember that I still have a stub section of my colon attached at the distal end that was left intact during my initial resection when part of my sigmoid colon was removed. The second surgery involved the removal of all of my colon upstream of the section that was removed during the first procedure, but the distal stub was left intact, due to complications during the surgery.
Now one could argue that I am having a celiac reaction during those challenges (because for all I know, I might be a celiac — I was never tested for celiac disease). But I'm not talking about reactions to gluten (though I do still react to gluten) — I'm talking about reacting to any of my known food sensitivities.
So normally, if I ingest a known trigger, the D will be limited to the output of the ileostomy. The stub is unaffected. Why? Because in a gut that is well-healed, T-cell reactions take a relatively long time to develop to a level where they will trigger a reaction. And I'm not naive enough to continue eating a food that causes a reaction, because I realize that in the long run, this is asking for some real trouble (in the form of a major T-cell-based reaction). This is one of the reasons why I am working on a book that questions conventional thinking about the inflammation involved in MC reactions. IMO, mast cell activity plays a primary role in some of these reactions, and I'm thinking that the mast cell reactions are most likely triggered virtually anywhere in the GI tract, rather than just in the large bowel.
If you carefully read my description of the reaction that I experienced as a result of the second kidney stone, you can see that it took a significant amount of time (3 weeks) for the inflammation (from the passage of the kidney stones) to reach a level where it triggered a reaction in the remaining stub of my colon. That was very likely a T-cell reaction, because it took so long to develop (and it required more than a single initial inflammation episode), and most importantly, the reaction occurred in the remaining stub of my colon. But the point is, the inflammation finally reached a level where it triggered an obvious (to me at least) MC reaction in that stub of a colon that had been disconnected from my gut for over 9 years. Watery D from a disconnected stub of a colon could only be attributed to MC. There is no other possible explanation. Is there? I realize that most physicians would insist that it's impossible, but hey, I was there, so I know that it is indeed possible.
I hope that I've done an adequate job of explaining what I believe to be the mechanism behind that reaction. Here's a link to my original description of the reaction while it was in progress.
Can Kidney Stones Trigger an MC Reaction?
But in addition to that unusual event, I maintain that MC reactions are not simply a result of T-cell reactions in the colon. They can also be triggered by mast cell reactions, and those mast cell reactions can presumably occur in either the small or large bowel. IOW just because lymphocyte counts in the mucosal lining of the colon are used as a diagnostic marker for LC, does not mean that other reaction mechanisms may not be present.
I suspect that those of us who are not susceptible to mast cell reactions are not as likely to always have prompt reactions to ingested food sensitivities if our gut is well-healed. Similar to what happens with celiac disease, we may have to build up a sufficient level of inflammation due to lymphocyte infiltration that exceeds our personal threshold at which a reaction is triggered, and this can take weeks or months, in some cases (if our gut is healed to begin with). But for those of us who have not accrued extensive healing, and/or we are vulnerable to mast cell activation disorder, reactions can always occur promptly after exposure to an ingested antigen. IOW, MC is a much more complex syndrome than is generally recognized, IMO.
And as far as the satellite symptoms such as brain fog, arthritis, fatigue, etc., are concerned, all but the fatigue are almost surely caused by increased intestinal permeability, rather than by MC itself, and typically they do not present immediately at the first signs of an MC reaction. Instead they tend to develop if/when a reaction continues for more than just a single day. Of course this is all just my strictly unprofessional opinion, and I could be all wet.
Love,
Tex
That's a very good question. And of course my first point is that MC is improperly named and/or improperly described in the medical literature, because there are volumes of research data that clearly show that the disease can affect not only both the large and small bowel, but other parts of the digestive tract as well. But in the example you noted, I did indeed have inflammation of the colon, as you will see below. I hope that I can explain my line of reasoning in a way that makes sense, because I should already be in bed, so I may accidentally leave out some important points, but here goes:
As you are aware, there are a few old medical articles that conclude that diversion of the fecal stream (by means of an ileostomy) cures MC. I have long maintained that those articles are bogus. Remember the lady who joined us roughly 4 or 5 years ago, who was persuaded by her doctors to agree to an ileostomy as a treatment for her MC that was refractive to treatment by other means? We tried in vain to persuade her not to agree to the procedure, but she went ahead anyway. And sadly, just as we feared, the procedure made no difference. She continued to react.
Since I have an ileostomy, it is rather easy for me to verify that the claims in those old articles don't hold up to even the simplest of tests. If I eat any of the triggers that caused me to react prior to my resection procedure, I still react with D (through the stoma), so this supports our contention that MC can affect either the large or small bowel.
Remember that I still have a stub section of my colon attached at the distal end that was left intact during my initial resection when part of my sigmoid colon was removed. The second surgery involved the removal of all of my colon upstream of the section that was removed during the first procedure, but the distal stub was left intact, due to complications during the surgery.
Now one could argue that I am having a celiac reaction during those challenges (because for all I know, I might be a celiac — I was never tested for celiac disease). But I'm not talking about reactions to gluten (though I do still react to gluten) — I'm talking about reacting to any of my known food sensitivities.
So normally, if I ingest a known trigger, the D will be limited to the output of the ileostomy. The stub is unaffected. Why? Because in a gut that is well-healed, T-cell reactions take a relatively long time to develop to a level where they will trigger a reaction. And I'm not naive enough to continue eating a food that causes a reaction, because I realize that in the long run, this is asking for some real trouble (in the form of a major T-cell-based reaction). This is one of the reasons why I am working on a book that questions conventional thinking about the inflammation involved in MC reactions. IMO, mast cell activity plays a primary role in some of these reactions, and I'm thinking that the mast cell reactions are most likely triggered virtually anywhere in the GI tract, rather than just in the large bowel.
If you carefully read my description of the reaction that I experienced as a result of the second kidney stone, you can see that it took a significant amount of time (3 weeks) for the inflammation (from the passage of the kidney stones) to reach a level where it triggered a reaction in the remaining stub of my colon. That was very likely a T-cell reaction, because it took so long to develop (and it required more than a single initial inflammation episode), and most importantly, the reaction occurred in the remaining stub of my colon. But the point is, the inflammation finally reached a level where it triggered an obvious (to me at least) MC reaction in that stub of a colon that had been disconnected from my gut for over 9 years. Watery D from a disconnected stub of a colon could only be attributed to MC. There is no other possible explanation. Is there? I realize that most physicians would insist that it's impossible, but hey, I was there, so I know that it is indeed possible.
I hope that I've done an adequate job of explaining what I believe to be the mechanism behind that reaction. Here's a link to my original description of the reaction while it was in progress.
Can Kidney Stones Trigger an MC Reaction?
But in addition to that unusual event, I maintain that MC reactions are not simply a result of T-cell reactions in the colon. They can also be triggered by mast cell reactions, and those mast cell reactions can presumably occur in either the small or large bowel. IOW just because lymphocyte counts in the mucosal lining of the colon are used as a diagnostic marker for LC, does not mean that other reaction mechanisms may not be present.
I suspect that those of us who are not susceptible to mast cell reactions are not as likely to always have prompt reactions to ingested food sensitivities if our gut is well-healed. Similar to what happens with celiac disease, we may have to build up a sufficient level of inflammation due to lymphocyte infiltration that exceeds our personal threshold at which a reaction is triggered, and this can take weeks or months, in some cases (if our gut is healed to begin with). But for those of us who have not accrued extensive healing, and/or we are vulnerable to mast cell activation disorder, reactions can always occur promptly after exposure to an ingested antigen. IOW, MC is a much more complex syndrome than is generally recognized, IMO.
And as far as the satellite symptoms such as brain fog, arthritis, fatigue, etc., are concerned, all but the fatigue are almost surely caused by increased intestinal permeability, rather than by MC itself, and typically they do not present immediately at the first signs of an MC reaction. Instead they tend to develop if/when a reaction continues for more than just a single day. Of course this is all just my strictly unprofessional opinion, and I could be all wet.
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.
Polly,
One more thought. A reaction caused by inflammation generated external to the intestines (originating within the renal system) in a stub of a colon that has been disconnected from the proximal digestive tract for 9 years would seem to not only dispute the commonly-repeated speculation that MC may be caused by luminal agents, such as pathogens or toxins in the fecal stream, but it also opens up a whole new spectrum of possible causes for MC.
Of course during that period of time, there was another potential source of inflammation, namely overtreatment of hypothyroidism (resulting in hyperthyroidism symptoms). Presumably this (together with a chronic magnesium deficiency problem) was the likely cause of the kidney stones in the first place. And to add another layer of complexity to this logic, consider that the dose of Armour that I was taking had been working just fine for at least 8 years. But suddenly my TSH began to decline, and when it dropped to 0.28 in October of 2014, that's when the kidney stones showed up. By February of 2015, my TSH was 0.07, and I was having major hyperthyroid symptoms (inability to sleep because of anxiety, panic attack-like symptoms, elevated heart rate, erratic BP problems, etc.). Of course these are also symptoms of magnesium deficiency, so not only did that surely exacerbate the symptoms, but also complicated the analysis of the problem/s.
Though I certainly have no proof, I'm convinced that this change in my thyroid response was due to resolving methylation issues by taking Metanx. It took years of taking Metanx, and sometimes experimenting with the dosage, to resolve (or at least improve) the problem, but it now appears to me that my initial hypothyroid symptoms were caused by epigenetic changes to my body chemistry (methylation processes) as a result of the surgery. Presumably the anesthetic may have been responsible, but all the antibiotics that were used because I didn't have time to clean out prior to an emergency colon resection might have played a role also, because as we all know, gut bacteria can alter gene expression. And the Metanx helped to resolve the methylation problems.
Remember that I have had breathing problems ("ideopathic" shortness of breath ever since my first surgery in November of 2005). It became slightly worse after my second surgery, so I'm guessing that either the anesthetic or one or more of the antibiiotics used somehow caused a permanent antagonism of magnesium absorption. In fact, one of the reasons why I was prescribed treatment for hypothyroidism in the first place was because of hypothyroid symptoms that began soon after that first surgery. So I can't be sure if the symptoms were actually due to an actual primary thyroid issue (my Free T4 was well below range), or a secondary issue such as a magnesium deficiency or methylation issues. With that many variables, the problem was likely the result of a combination of factors. At any rate, consider what I wrote to someone yesterday in an email after she asked if I had recovered from the problems that I had earlier in the year.
Of course most of this is speculation/educated guessing, but what else can we do. There are no RCTs that directly apply to unusual situations such as this. But to get back to the topic of your question, the more I look at all the aspects of this disease, the more it appears as though MC is a symptom (of inflammation) rather than a disease.
Love,
Tex
One more thought. A reaction caused by inflammation generated external to the intestines (originating within the renal system) in a stub of a colon that has been disconnected from the proximal digestive tract for 9 years would seem to not only dispute the commonly-repeated speculation that MC may be caused by luminal agents, such as pathogens or toxins in the fecal stream, but it also opens up a whole new spectrum of possible causes for MC.
Of course during that period of time, there was another potential source of inflammation, namely overtreatment of hypothyroidism (resulting in hyperthyroidism symptoms). Presumably this (together with a chronic magnesium deficiency problem) was the likely cause of the kidney stones in the first place. And to add another layer of complexity to this logic, consider that the dose of Armour that I was taking had been working just fine for at least 8 years. But suddenly my TSH began to decline, and when it dropped to 0.28 in October of 2014, that's when the kidney stones showed up. By February of 2015, my TSH was 0.07, and I was having major hyperthyroid symptoms (inability to sleep because of anxiety, panic attack-like symptoms, elevated heart rate, erratic BP problems, etc.). Of course these are also symptoms of magnesium deficiency, so not only did that surely exacerbate the symptoms, but also complicated the analysis of the problem/s.
Though I certainly have no proof, I'm convinced that this change in my thyroid response was due to resolving methylation issues by taking Metanx. It took years of taking Metanx, and sometimes experimenting with the dosage, to resolve (or at least improve) the problem, but it now appears to me that my initial hypothyroid symptoms were caused by epigenetic changes to my body chemistry (methylation processes) as a result of the surgery. Presumably the anesthetic may have been responsible, but all the antibiotics that were used because I didn't have time to clean out prior to an emergency colon resection might have played a role also, because as we all know, gut bacteria can alter gene expression. And the Metanx helped to resolve the methylation problems.
Remember that I have had breathing problems ("ideopathic" shortness of breath ever since my first surgery in November of 2005). It became slightly worse after my second surgery, so I'm guessing that either the anesthetic or one or more of the antibiiotics used somehow caused a permanent antagonism of magnesium absorption. In fact, one of the reasons why I was prescribed treatment for hypothyroidism in the first place was because of hypothyroid symptoms that began soon after that first surgery. So I can't be sure if the symptoms were actually due to an actual primary thyroid issue (my Free T4 was well below range), or a secondary issue such as a magnesium deficiency or methylation issues. With that many variables, the problem was likely the result of a combination of factors. At any rate, consider what I wrote to someone yesterday in an email after she asked if I had recovered from the problems that I had earlier in the year.
When I was a kid, I had severe asthma, so I'm very familiar with how it feels. The breathing problem I had for over 9 years felt just like asthma, except that there was no wheezing. As with asthma, I was always conscious of my breathing whenever I was having an episode, and breathing was labored. I couldn't take a deep breath, and sometimes it became very tiring. My doctors could never detect that anything was abnormal about my breathing, despite carefully listening to my breathing through their stethoscopes. It was almost as frustrating as having MC when your GI specialist fails to take biopsies during a colonoscopy exam.Yes, I seem to be fully recovered from the reaction I had to the antibiotic a month or so ago, and now that I am taking the extra magnesium (on top of the double RDA magnesium supplement that I was taking previously), my breathing is better than it has ever been since my first surgery (almost 10 years ago). Apparently I have a serious magnesium malabsorption problem that was initially triggered by the anesthetic used during my 2 surgeries (the second surgery was 5 years ago). By taking 1,200 mg of magnesium per day (more or less, since some of it is applied topically on some days), I can breathe normally again. After almost 10 years of being short of breath, being able to breath normally again almost seems like a miracle.
It seems strange to say this, but if I hadn't had the adverse reaction to the antibiotic (which finished depleting my magnesium supply), I probably never would have figured out that my breathing problem (and some other symptoms) was/were due to a chronic magnesium deficiency (because I was already taking a lot of magnesium). So I owe my relief to that antibiotic reaction. As I often say, "There's almost always a silver lining to every cloud". Sometimes we have to search for it, but it is virtually always there, somewhere.
Of course most of this is speculation/educated guessing, but what else can we do. There are no RCTs that directly apply to unusual situations such as this. But to get back to the topic of your question, the more I look at all the aspects of this disease, the more it appears as though MC is a symptom (of inflammation) rather than a disease.
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.
Hi Tex,
Sorry I haven't gotten back to you sooner. I have been out-of-town. Thank you for taking the time to answer my question so thoughtfully and completely. I will need to study your comments and digest (pun intended) them, and then I will get back to you. This is such an interesting subject, isn't it? With everything we DO know about MC, we don't really understand the most basic mechanisms involved.
Love,
Polly
Sorry I haven't gotten back to you sooner. I have been out-of-town. Thank you for taking the time to answer my question so thoughtfully and completely. I will need to study your comments and digest (pun intended) them, and then I will get back to you. This is such an interesting subject, isn't it? With everything we DO know about MC, we don't really understand the most basic mechanisms involved.
Love,
Polly
Blessed are they who can laugh at themselves, for they shall never cease to be amused.
Hi Tex,
OK, I have been thinking some. Please explain more about the remaining stub you have. Do you know how long it is? I am trying to picture it - was the stub the proximal part of the sigmoid colon? So apparently there is no connection between your stub and the ileostomy, right? So, if the colonic stub were inflamed, I can't see how it could lead to watery D.
I agree 100% that it is generalized inflammation that is involved. And mast cells figure prominently, I think. We always think of the secretory diarrhea as occurring from inflammation in the colon, but I believe increased motility in the proximal part of the GI tract may be just as important a cause of the D. With increased speed in the small bowel, important minerals, electrolytes, and nutrients would not be absorbed, and this could set the stage for inflammation and poor water absorption in the colon. IOW, I wonder what came first? The colonic inflammation could be simply a reaction to the process and not the cause. For example, bile salts are normally absorbed in the terminal ileum. But with increased motility, there isn't enough time for adequate absorption. So this can allow a large amount of those corrosive bile salts to travel into the colon and damage the colonic mucosa. I am having an issue with this currently.....and some studies I saw said up to 43% of MCers may have a problem with bile salts diarrhea (LC more than CC, BTW).
So I guess what I am saying is that I think MOTILITY is an important and under-appreciated part of the disease process - from mouth to anus. Another example - many folks experience delayed gastric emptying or even frank gastroparesis. Now this may be related to stomach acid levels, but again, I wonder what the basic mechanism is that sets this all in motion.
Up 'til now, motility problems have mostly been ascribed to IBS, but I think they apply to MC equally. And I find it interesting that motility is very much related to the brain.....to stress. As you know, I have always been one to have to run to the loo whenever I am scared or stressed - long before I got MC.
Those are my initial thoughts.
Love,
Polly
OK, I have been thinking some. Please explain more about the remaining stub you have. Do you know how long it is? I am trying to picture it - was the stub the proximal part of the sigmoid colon? So apparently there is no connection between your stub and the ileostomy, right? So, if the colonic stub were inflamed, I can't see how it could lead to watery D.
I agree 100% that it is generalized inflammation that is involved. And mast cells figure prominently, I think. We always think of the secretory diarrhea as occurring from inflammation in the colon, but I believe increased motility in the proximal part of the GI tract may be just as important a cause of the D. With increased speed in the small bowel, important minerals, electrolytes, and nutrients would not be absorbed, and this could set the stage for inflammation and poor water absorption in the colon. IOW, I wonder what came first? The colonic inflammation could be simply a reaction to the process and not the cause. For example, bile salts are normally absorbed in the terminal ileum. But with increased motility, there isn't enough time for adequate absorption. So this can allow a large amount of those corrosive bile salts to travel into the colon and damage the colonic mucosa. I am having an issue with this currently.....and some studies I saw said up to 43% of MCers may have a problem with bile salts diarrhea (LC more than CC, BTW).
So I guess what I am saying is that I think MOTILITY is an important and under-appreciated part of the disease process - from mouth to anus. Another example - many folks experience delayed gastric emptying or even frank gastroparesis. Now this may be related to stomach acid levels, but again, I wonder what the basic mechanism is that sets this all in motion.
Up 'til now, motility problems have mostly been ascribed to IBS, but I think they apply to MC equally. And I find it interesting that motility is very much related to the brain.....to stress. As you know, I have always been one to have to run to the loo whenever I am scared or stressed - long before I got MC.
Those are my initial thoughts.
Love,
Polly
Blessed are they who can laugh at themselves, for they shall never cease to be amused.
All I know is that approximately 17 or 18 cm (roughly 7 inches) of my sigmoid colon was removed (due to a stenosis attributed to diverticulitis) during the first surgery, which left me with a colostomy attached to the distal end of the remaining intact (still functional) section of the colon (presumably the distal end of the transverse colon), and the disconnected stub still attached to the rectum. And you are correct, the stub has always remained totally disconnected from the functional part of the GI tract.Polly wrote:OK, I have been thinking some. Please explain more about the remaining stub you have. Do you know how long it is? I am trying to picture it - was the stub the proximal part of the sigmoid colon? So apparently there is no connection between your stub and the ileostomy, right? So, if the colonic stub were inflamed, I can't see how it could lead to watery D.
Here is how (IMO) the stub can react with watery "D": Remember that the type of D that distinguishes active MC (and other IBDs) is secretory diarrhea. And as you know:
Secretory diarrhea.Secretory diarrhea can result from bacterial toxins, reduced absorptive surface area caused by disease or resection, luminal secretagogues (such as bile acids or laxatives), circulating secretagogues (such as various hormones, drugs, and poisons), and medical problems that compromise regulation of intestinal function.
With MC, secretory diarrhea is almost surely caused by a malabsorption problem (the equivalent of reduced absorptive surface area), but of course bile acids may also contribute (but remember that the reason why they are still there is because they were not properly absorbed). Before IBDs were understood, and a working knowledgebase became available (IOW historically) this type of diarrhea was typically associated with toxins produced by certain pathogenic bacteria (such as Staphylococcus, Escherichia coli, and Vibrio cholerae). IMO this may well be the primary reason why so many physicians/researchers suspect that MC may be caused by a pathogenic bacteria (another if-you-hear-hoofbeats type of assumption/association).
And most importantly, secretory diarrhea occurs when the body is releasing water into the bowel. And what is the source of this water? The bloodstream, of course. Water is absorbed into the bloodstream from the colon when the digestive system is working properly, and water is infused back into the colon from the bloodstream, when secretory D is present. And here is some additional information from Wikipedia that explains why secretory D can be so dangerously dehydrating, for anyone reading this who might be interested. The red emphasis is mine, of course.
DiarrheaSecretory diarrhea means that there is an increase in the active secretion, or there is an inhibition of absorption. There is little to no structural damage. The most common cause of this type of diarrhea is a cholera toxin that stimulates the secretion of anions, especially chloride ions. Therefore, to maintain a charge balance in the lumen, sodium is carried with it, along with water. In this type of diarrhea intestinal fluid secretion is isotonic with plasma even during fasting.[11] It continues even when there is no oral food intake.
Remember that the stub remaining from my colon is still nourished by the same vascular system that services the remaining digestive organs and the rest of the body. IOW, just because the stub's lumen is disconnected from the active part of the digestive system does not disqualify it from secretory D, because it is serviced by the same vascular system as the rest of the digestive system, and most importantly, it is still controlled by the same enteric nervous system as the rest of the digestive system. And with secretory D, no oral food intake is necessary. Right? IOW, all that the stub could possibly produce was water and mucin (mucin becomes mucus after contact with water), and that's exactly what it did.
Because of the mechanisms by which the various types of D occur, IMO D always originates in the small intestine, because that is precisely where malabsorption of the electrolytes that trigger D originates. If the small intestine does not absorb these electrolytes, then they cannot be absorbed in the colon, either. In fact, if I recall correctly, it is known that if the small intestine fails to absorb (or reabsorb) at least a certain minimum amount of these electrolytes, then not only will they remain in the fecal stream, promoting D in both the small and large intestines, but their increased presence will trigger the infusion of additional electrolytes into the colon, thereby intensifying the D and escalating the dehydration risk. This is just my opinion, but I believe (based on the constraints imposed by the known mechanisms by which D is triggered), that if D is not present in the small intestine, it will not be present in the colon, either.Polly wrote:IOW, I wonder what came first? The colonic inflammation could be simply a reaction to the process and not the cause.
Polly wrote:Another example - many folks experience delayed gastric emptying or even frank gastroparesis. Now this may be related to stomach acid levels, but again, I wonder what the basic mechanism is that sets this all in motion.
I'm just thinking out loud here, but I have a hunch that delayed gastric emptying/gastroparesis probably occurs because the enteric nervous system has not received a "ready" signal from the pancreas, informing it that the pancreas can supply enough bicarbonate to at least meet certain minimal digestive system "safety" requirements. I'm guessing that bicarbonate would be a critical ingredient, because surely the enteric nervous system would not allow the pyloric sphincter to release the chyme from the stomach if the pH of the chyme were at a level of 2 or 3 (or less), for example, and not enough bicarbonate were available to at least neutralize most of the acidity.
Such a mistake would destroy the lining of the duodenum in a very short period of time (if at least a certain minimal amount of bicarbonate were not immediately available to neutralize the acidity of the chyme). IOW, I believe that this is just a feature of the enteric nervous system designed to protect the integrity of the small intestine from accidental "digestion" by stomach acid. The fact that gastroparesis is associated with diabetes and MC (though the members of this discussion board are probably the only people in the world who recognize that gastroparesis is associated with MC) is no conincidence, IMO, because both issues are associated with (or can cause) pancreatic malfunction. Right?
At least that's the way I view these issues.
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.
Hi Tex,
Excellent discussion of D/secretory D. Actually, this morning when I read your posts, I was in a hurry and scanned them quickly. I thought you were saying that you had a flare from the kidney stones because you still had some colon left ---but now that I read carefully, you were saying the opposite! (That's why I was trying to find out more about that colon stump you have left......to try to figure out some mechanism for how that could cause a flare). Now I understand what you meant and am complete agreement with you about MC not needing a colon. After all, you are the poster boy for that fact! BTW, the big university medical centers are still to this day recommending fecal stream diversion as a last ditch attempt to cure MC.
Do you think there are any clues when we look at LC vs. CC? I know they are clinically indistinguishable, but there are some differences at the cellular level. I believe the secretory D in LC involves sodium excretion, as opposed to chloride/bicarb excretion in CC. Also, CCers are more likely to have other A.I. diseases.
Gastroparesis aside, how much do you think the enteric nervous system influences MC?
Love,
Polly
Excellent discussion of D/secretory D. Actually, this morning when I read your posts, I was in a hurry and scanned them quickly. I thought you were saying that you had a flare from the kidney stones because you still had some colon left ---but now that I read carefully, you were saying the opposite! (That's why I was trying to find out more about that colon stump you have left......to try to figure out some mechanism for how that could cause a flare). Now I understand what you meant and am complete agreement with you about MC not needing a colon. After all, you are the poster boy for that fact! BTW, the big university medical centers are still to this day recommending fecal stream diversion as a last ditch attempt to cure MC.
Do you think there are any clues when we look at LC vs. CC? I know they are clinically indistinguishable, but there are some differences at the cellular level. I believe the secretory D in LC involves sodium excretion, as opposed to chloride/bicarb excretion in CC. Also, CCers are more likely to have other A.I. diseases.
Gastroparesis aside, how much do you think the enteric nervous system influences MC?
Love,
Polly
Blessed are they who can laugh at themselves, for they shall never cease to be amused.
Polly,
Great questions. I've never given any thought to the implications that might be associated with the differences between LC and CC. But you're right, there is probably a very good reason for the different markers that are involved. There's a reason for everything. I'll have to give that some thought. Likewise on the question about the enteric nervous system. Just as the brain diverts blood flow to the core of the body when hypothermia develops, surely the enteric nervous system initiates drastic changes within the digestive system when certain digestion processes become corrupt.
Love,
Tex
Great questions. I've never given any thought to the implications that might be associated with the differences between LC and CC. But you're right, there is probably a very good reason for the different markers that are involved. There's a reason for everything. I'll have to give that some thought. Likewise on the question about the enteric nervous system. Just as the brain diverts blood flow to the core of the body when hypothermia develops, surely the enteric nervous system initiates drastic changes within the digestive system when certain digestion processes become corrupt.
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.
I want to add to this discussion (because you mentioned the mast cell issues) that the more I read about oxalates, the more I believe it is related to our struggle.
The ladies on the FB, Trying Low Oxalates group and the Yahoo group are at the forefront of the research on this topic. Susan Owens (founder) is an amazing woman who can put 2 and 2 together when the medical profession ignores it!
Oxalates can set off reactions in any soft area of the body....not just joint pain, but the heart, even the gut....some speculation about it causing leaky gut because the oxalates are like charred pieces of glass that tear away at different soft tissues in the body.
Tex....it may be worth looking into for another piece to this complicated puzzle.
Have a good day!
The ladies on the FB, Trying Low Oxalates group and the Yahoo group are at the forefront of the research on this topic. Susan Owens (founder) is an amazing woman who can put 2 and 2 together when the medical profession ignores it!
Oxalates can set off reactions in any soft area of the body....not just joint pain, but the heart, even the gut....some speculation about it causing leaky gut because the oxalates are like charred pieces of glass that tear away at different soft tissues in the body.
Tex....it may be worth looking into for another piece to this complicated puzzle.
Have a good day!
Linda :)
LC Oct. 2012
MTHFR gene mutation and many more....
LC Oct. 2012
MTHFR gene mutation and many more....
Hi Linda,
Polly started the discussion about oxalates on this board over 9 years ago, and the topic continues to come up regularly. There's no question that oxalates almost surely play a significant role in our digestive issues (depending on our diet). Here are a couple of links to some of the earliest discussions:
Oxalates
Mechanisms Behind The Leaky Gut
The main link in the first post in that thread is no longer active, but the discussion is still interesting. Susan Owens has long been a leader in oxalate research (presumably since long before FB came along) Here is a link to an excellent and extremely comprehensive article that you are probably very familiar with. I wonder if this article might have been the target of the link that no longer works.
Low Oxalate Diet
But in the overall realm of the etiology of MC, I have a hunch that oxalates are very likely just one more addition to the very long list of issues that can contribute to the development and/or perpetuation of the inflammation that causes MC. For some of us oxalates may be much more significant than for others, depending on our individual sensitivity to them, our current level of intestinal damage, and the level (volume) of their presence in our diet. Personally, I have always tended to minimize the foods in this category in my diet. I'm not sure if that was coincidence or if I actually had a reason (based on symptoms).
Tex
Polly started the discussion about oxalates on this board over 9 years ago, and the topic continues to come up regularly. There's no question that oxalates almost surely play a significant role in our digestive issues (depending on our diet). Here are a couple of links to some of the earliest discussions:
Oxalates
Mechanisms Behind The Leaky Gut
The main link in the first post in that thread is no longer active, but the discussion is still interesting. Susan Owens has long been a leader in oxalate research (presumably since long before FB came along) Here is a link to an excellent and extremely comprehensive article that you are probably very familiar with. I wonder if this article might have been the target of the link that no longer works.
Low Oxalate Diet
But in the overall realm of the etiology of MC, I have a hunch that oxalates are very likely just one more addition to the very long list of issues that can contribute to the development and/or perpetuation of the inflammation that causes MC. For some of us oxalates may be much more significant than for others, depending on our individual sensitivity to them, our current level of intestinal damage, and the level (volume) of their presence in our diet. Personally, I have always tended to minimize the foods in this category in my diet. I'm not sure if that was coincidence or if I actually had a reason (based on symptoms).
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.
Hi Polly,
I have to report that I haven't had any illuminating thoughts, or encountered any research that sheds any significant light on the reasons for the distinctions between LC and CC, but I'll continue to look for any clues.
Regarding your question about the enteric nervous system, I doubt that corruption in the enteric nervous system is responsible for the development of MC, if that's what you were suggesting. But of course, that's just my opinion, and opinions based on guesswork aren't worth much.
Love,
Tex
I have to report that I haven't had any illuminating thoughts, or encountered any research that sheds any significant light on the reasons for the distinctions between LC and CC, but I'll continue to look for any clues.
Regarding your question about the enteric nervous system, I doubt that corruption in the enteric nervous system is responsible for the development of MC, if that's what you were suggesting. But of course, that's just my opinion, and opinions based on guesswork aren't worth much.
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.
Thanks, Tex.
I am familiar with the site you mentioned and it is very Good information. Thanks for the old threads, too.
When I did a 24 hour urine test, my oxalates were at the high end of the range....but I had already started to lower them, because I had many symptoms described as high oxalate related issues. I think it has helped to eat low ox. There are so many other symptoms besides kidney stones that can be attributed to high ox. It's fascinating to read about....
I am familiar with the site you mentioned and it is very Good information. Thanks for the old threads, too.
When I did a 24 hour urine test, my oxalates were at the high end of the range....but I had already started to lower them, because I had many symptoms described as high oxalate related issues. I think it has helped to eat low ox. There are so many other symptoms besides kidney stones that can be attributed to high ox. It's fascinating to read about....
Linda :)
LC Oct. 2012
MTHFR gene mutation and many more....
LC Oct. 2012
MTHFR gene mutation and many more....
I agree. I've generally tried to avoid high-oxalate foods ever since I found out about them, 9 years ago.
The downside is that a lot of high-oxalate foods seem to be the best sources of vitamin K2, but that's the way the cookie crumbles, I suppose.
Tex
The downside is that a lot of high-oxalate foods seem to be the best sources of vitamin K2, but that's the way the cookie crumbles, I suppose.
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.
Yes, but we can supplement K2. I don't get a lot of it anyway, because it is in dairy foods. There are other dark leafy greens that we can eat on the low ox diet, like regular romaine, & gardens lettuces...just not spinach & chard.
The more ya know, the more you realize you don't know! We are complex human beings.....
We are enjoying warm but dryness in my neck of the woods.....you having too much rain there, Tex?
The more ya know, the more you realize you don't know! We are complex human beings.....
We are enjoying warm but dryness in my neck of the woods.....you having too much rain there, Tex?
Linda :)
LC Oct. 2012
MTHFR gene mutation and many more....
LC Oct. 2012
MTHFR gene mutation and many more....