Back on bile again
Moderators: Rosie, Stanz, Jean, CAMary, moremuscle, JFR, Dee, xet, Peggy, Matthew, Gabes-Apg, grannyh, Gloria, Mars, starfire, Polly, Joefnh
Back on bile again
I eas searching for information about what Dr. Teitelbaum thought about amalgams/mercury, etc. And what did I find...
Well, speaking of toxins and Dr. Teitelbaum, take a look at this article and notice that it's talking about bile. I mentioned in passing before that perhaps our bile is more toxic and thus causes damage, in other words not that we produce too much bile but that the bile is damaging.
Neurotoxins-Treatment Information Sheet
http://www.ei-resource.org/articles/cfs/cfs-art29.asp
So lets say that this is indeed the case, that our bile is more toxic. Why might that be? Infections, NSAIDs, acetomeniphin use, dysbiosis, heavy metals, chemicals, smoking. Aren't a bunch of these noted as causes of MC?
What damage might these toxins do? Damage to gallbladder (seems common for MCers), damage to upper and lower GI (might explain malabsorption issues, leaky gut, damage to colon, inflamation), low levels of glutathione (what detoxifies toxins), low levels of antioxidents. I wonder if it would also explain the damage done to other organs that use cholesterol or recycled bile (Adrenals to start with).
What other organs use cholesterol? I'm guessing that the sex organs do since they deal with producing the sex sterols. I'd also guess that the kidneys are involved because of Vitamin D. Here's another, isn't the brain composed of or contain a lot of cholesterol? Anyone know what else?
Besides the obvious, Colon and gallbladder, what other organs are comonly effected in MC?
Mike
Well, speaking of toxins and Dr. Teitelbaum, take a look at this article and notice that it's talking about bile. I mentioned in passing before that perhaps our bile is more toxic and thus causes damage, in other words not that we produce too much bile but that the bile is damaging.
Neurotoxins-Treatment Information Sheet
http://www.ei-resource.org/articles/cfs/cfs-art29.asp
So lets say that this is indeed the case, that our bile is more toxic. Why might that be? Infections, NSAIDs, acetomeniphin use, dysbiosis, heavy metals, chemicals, smoking. Aren't a bunch of these noted as causes of MC?
What damage might these toxins do? Damage to gallbladder (seems common for MCers), damage to upper and lower GI (might explain malabsorption issues, leaky gut, damage to colon, inflamation), low levels of glutathione (what detoxifies toxins), low levels of antioxidents. I wonder if it would also explain the damage done to other organs that use cholesterol or recycled bile (Adrenals to start with).
What other organs use cholesterol? I'm guessing that the sex organs do since they deal with producing the sex sterols. I'd also guess that the kidneys are involved because of Vitamin D. Here's another, isn't the brain composed of or contain a lot of cholesterol? Anyone know what else?
Besides the obvious, Colon and gallbladder, what other organs are comonly effected in MC?
Mike
Mike,
Every cell in the body requires cholesterol in its membranes. It's also the starting material from which the body makes vitamin D, and as you pointed out, steroid hormones and bile acids for digestion.
Like Crohn's, MC can affect any part of the GI tract, from mouth to anus. I don't think that it's very common for the stomach and parts above it to be involved, (other than mouth sores, etc.), but the small intestine is commonly involved. My feeling is that most of the effects on the other organs, (and joints, etc.), are consequences of LGS, rather than MC, per se, but that's just my opinion, and YMMV. Of course, LGS and MC are pretty much constant companions, during active episodes, for most/all of us. Sort of a chicken and egg thing, but I suspect that the LGS is the chicken, in this arrangement.
Lest someone misinterpret the list of factors conducive to MC that you mentioned, I feel motivated to point out that, to my knowledge at least, acetaminophen has not been demonstrated to cause MC, (or have I missed something?), and smoking is actually protective of MC, (in a sense). IOW, it's not smoking that causes MC, it's stopping a smoking habit. I hope I'm right about acetaminophen, because I use the stuff regularly, since it's the only OTC painkiller that I'm aware of that's generally conceded to be safe for MCers, (other than the risk of kidney failure. LOL).
I find your observations about glutathione to be extremely interesting, by the way. I wish I knew what my readings were, over the last ten years, but apparently it isn't routinely checked, during clinic/hospital visits.
Thanks for being so inquisitive, and finding all this stuff.
Tex
Every cell in the body requires cholesterol in its membranes. It's also the starting material from which the body makes vitamin D, and as you pointed out, steroid hormones and bile acids for digestion.
Like Crohn's, MC can affect any part of the GI tract, from mouth to anus. I don't think that it's very common for the stomach and parts above it to be involved, (other than mouth sores, etc.), but the small intestine is commonly involved. My feeling is that most of the effects on the other organs, (and joints, etc.), are consequences of LGS, rather than MC, per se, but that's just my opinion, and YMMV. Of course, LGS and MC are pretty much constant companions, during active episodes, for most/all of us. Sort of a chicken and egg thing, but I suspect that the LGS is the chicken, in this arrangement.
Lest someone misinterpret the list of factors conducive to MC that you mentioned, I feel motivated to point out that, to my knowledge at least, acetaminophen has not been demonstrated to cause MC, (or have I missed something?), and smoking is actually protective of MC, (in a sense). IOW, it's not smoking that causes MC, it's stopping a smoking habit. I hope I'm right about acetaminophen, because I use the stuff regularly, since it's the only OTC painkiller that I'm aware of that's generally conceded to be safe for MCers, (other than the risk of kidney failure. LOL).
I find your observations about glutathione to be extremely interesting, by the way. I wish I knew what my readings were, over the last ten years, but apparently it isn't routinely checked, during clinic/hospital visits.
Thanks for being so inquisitive, and finding all this stuff.
Tex
Sorry, didn't mean to imply that I thought acetaminophen caused MC, I was more mentioning the glutathione reducers and noticed that some were related to causes of MC. Though it is found in glutathione depletion unless one supplements with NAC (or I would assume eats foods that contain this or other parts of this amino acid). You're right, most places I found mentioned that one should take Tylenol/acetaminophen instead of NSAIDs. Though with that said one would wonder what this might mean for MC folks (or even other diseases where drs recommend tylenol instead of NSAIDs because it shows NSAIDs promote that disease) to go from one poisen to another. :(tex wrote:Lest someone misinterpret the list of factors conducive to MC that you mentioned, I feel motivated to point out that, to my knowledge at least, acetaminophen has not been demonstrated to cause MC, (or have I missed something?), and smoking is actually protective of MC, (in a sense). IOW, it's not smoking that causes MC, it's stopping a smoking habit. I hope I'm right about acetaminophen, because I use the stuff regularly, since it's the only OTC painkiller that I'm aware of that's generally conceded to be safe for MCers, (other than the risk of kidney failure. LOL).
As far as smoking goes I did find this, unless I'm misinterpreting the study it reads to me that smoking is a negative. I do remember reading that smoking is more likely to cause one to NOT get Crohn's Disease though.
http://www.ncbi.nlm.nih.gov/entrez/quer ... med_docsum
If anything this study shows that if one smokes you are more likely to get CC rather than LC. In fact another study of sisters who had MC, the smoker had CC whereas the non-smoker had LC. Since most studies seem to imply that CC is associated with more damage, or some that imply that LC progresses to CC might it be that in folks with CC they have less glutathione (smokers as an example) and thus more damage? Or a disease that progressed further?Twenty five per cent of patients with collagenous colitis compared with 14% of patients with lymphocytic colitis were active smokers; only 8.3% of patients with collagenous colitis had stopped smoking compared with 23% of patients with lymphocytic colitis (p=0.013).
Here's another curiousity. In folks with lower acid production they find lower glutathione levels, which causes which I'm not sure, but given that low acid production would mean less protein breakdown and thus less amino acids for the body to digest and then to take it further less components to make glutathione. And given that proton pump inhibitors are one of the things mentioned in causing problems for digestive diseases. Microscopic colitis being one of them.
You still could probably be checked just to see. Would be interesting to know. :) Given what I've read so for I would imagine that soon enough this will be one of those important things to check for, at least with certain symptoms.I find your observations about glutathione to be extremely interesting, by the way. I wish I knew what my readings were, over the last ten years, but apparently it isn't routinely checked, during clinic/hospital visits.
Thanks for being so inquisitive, and finding all this stuff.
Tex
Mike
Hi Friends,
This is so interesting. Have never had my glutathione checked but will definitely have it checked at my April appointment. It feels like you are talking about my decline...gallbladder disease since teen years and Prilosec for 6 years to deal with the pain. Then a hysterectomy to further screw up the endocrine system. My body is actually doing fairly well given all it has been through.
I am off to Ohio tomorrow to see parents so I won't be around for a week or so. I hate missing all this great info. Will have fun catching up when I get back. Take care friends.
Love,
Cristi
This is so interesting. Have never had my glutathione checked but will definitely have it checked at my April appointment. It feels like you are talking about my decline...gallbladder disease since teen years and Prilosec for 6 years to deal with the pain. Then a hysterectomy to further screw up the endocrine system. My body is actually doing fairly well given all it has been through.
I am off to Ohio tomorrow to see parents so I won't be around for a week or so. I hate missing all this great info. Will have fun catching up when I get back. Take care friends.
Love,
Cristi
Well, I'm running contrary to the pack again. I smoked for 40 years. I got MC after I stopped smoking and my diagnosis was LC not CC.
I'm not trying to be contrary, just pointing out the differences. I enjoy all the research you all do.
Love, Shirley
I'm not trying to be contrary, just pointing out the differences. I enjoy all the research you all do.
Love, Shirley
When the eagles are silent, the parrots begin to jabber"
-- Winston Churchill
-- Winston Churchill
Two comments:
#1 - I smoke and have for over 25 years - I have MC
#2 - the acid production - I'm confused - I take Nexium due to EXTREME acid reflux - if we are discussing that we produce "not enough acid", what's the deal with the reflux? Help me please!
Thanks
Mars
#1 - I smoke and have for over 25 years - I have MC
#2 - the acid production - I'm confused - I take Nexium due to EXTREME acid reflux - if we are discussing that we produce "not enough acid", what's the deal with the reflux? Help me please!
Thanks
Mars
"Let us rise up and be thankful, for if we didn't learn a lot today, at least we learned a little, and if we didn't learn a little, at least we didn't get sick, and if we got sick, at least we didn't die; so, let us all be thankful." -- Buddha
Mars,
The sphincter between the stomach and esophagus requires a low pH, (very acidic), in order to stay locked closed. It actually senses the pH level for it's cue as to how it perceives it is expected to perform. If the pH of the stomach contents is too high, (not acid enough), the sphincter will tend to relax, somwehat.
IOW, it operates on the principle that very acidic stomach contents, require a much more secure seal, than would be the case with a weaker acidity reading. When you think about it, this is quite logical, since a tighter seal is more important, (to guard against aesophageal burn), when the pH is the lowest.
There's a thread somewhere, where we discussed this previously, if you want to read more from some reference sources. The proper keywords to find it don't come to mind at the moment, but I'll search for it, if you would like to read it.
Love,
Tex
The sphincter between the stomach and esophagus requires a low pH, (very acidic), in order to stay locked closed. It actually senses the pH level for it's cue as to how it perceives it is expected to perform. If the pH of the stomach contents is too high, (not acid enough), the sphincter will tend to relax, somwehat.
IOW, it operates on the principle that very acidic stomach contents, require a much more secure seal, than would be the case with a weaker acidity reading. When you think about it, this is quite logical, since a tighter seal is more important, (to guard against aesophageal burn), when the pH is the lowest.
There's a thread somewhere, where we discussed this previously, if you want to read more from some reference sources. The proper keywords to find it don't come to mind at the moment, but I'll search for it, if you would like to read it.
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 is one of those topics:
http://www.perskyfarms.com/phpBB2/viewt ... cid+reflux
This is a good reference that Matthew cites:
http://www.vrp.com/art/784.asp
and here is the topic that Matthew mentioned in his first post in the topic mentioned above:
http://www.perskyfarms.com/phpBB2/viewt ... =difficile
Tex
http://www.perskyfarms.com/phpBB2/viewt ... cid+reflux
This is a good reference that Matthew cites:
http://www.vrp.com/art/784.asp
and here is the topic that Matthew mentioned in his first post in the topic mentioned above:
http://www.perskyfarms.com/phpBB2/viewt ... =difficile
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.
Mike,
To add to the illusion that it's possible to find studies which "prove" just about anything one desires to prove, (LOL), here is a quote from a study on smoking and UC:
http://www.ncbi.nlm.nih.gov/entrez/quer ... t=Abstract
The key here is the fact that smoking increases mucus, which helps to protect the colon.
From The New England Journal of Medicine:
http://content.nejm.org/cgi/content/extract/330/12/856
and one more:
http://www.forces.org/evidence/carol/carol40.htm
Tex
To add to the illusion that it's possible to find studies which "prove" just about anything one desires to prove, (LOL), here is a quote from a study on smoking and UC:
From:Significant clinical benefit was seen, indicating nicotine may be both useful therapeutically and the component of tobacco smoke that acts to protect against colitis.
http://www.ncbi.nlm.nih.gov/entrez/quer ... t=Abstract
The key here is the fact that smoking increases mucus, which helps to protect the colon.
From The New England Journal of Medicine:
From:Smokers are less likely to have ulcerative colitis, smoking may ameliorate its clinical manifestations, and the onset of colitis is often associated with the cessation of smoking.
http://content.nejm.org/cgi/content/extract/330/12/856
and one more:
from:By contrast, about 90% of the victims of ulcerative colitis are non-smokers. They are at 3.5 times greater risk than smokers.
In ex-smokers, onset is nearly always after quitting smoking. Smoking appears to have a protective effect against the development of this disease, and also reduces its severity.
http://www.forces.org/evidence/carol/carol40.htm
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.
Right, but we're talking about MC and not UC. According to the study I referenced above they associate smoking or even stop smoking to being a potential cause. And heck given the statistics in that study it appears that smoking is more a cause than NSAIDs.tex wrote:Mike,
To add to the illusion that it's possible to find studies which "prove" just about anything one desires to prove, (LOL), here is a quote from a study on smoking and UC:
From:Significant clinical benefit was seen, indicating nicotine may be both useful therapeutically and the component of tobacco smoke that acts to protect against colitis.
http://www.ncbi.nlm.nih.gov/entrez/quer ... t=Abstract
The key here is the fact that smoking increases mucus, which helps to protect the colon.
From The New England Journal of Medicine:
From:Smokers are less likely to have ulcerative colitis, smoking may ameliorate its clinical manifestations, and the onset of colitis is often associated with the cessation of smoking.
http://content.nejm.org/cgi/content/extract/330/12/856
and one more:
from:By contrast, about 90% of the victims of ulcerative colitis are non-smokers. They are at 3.5 times greater risk than smokers.
In ex-smokers, onset is nearly always after quitting smoking. Smoking appears to have a protective effect against the development of this disease, and also reduces its severity.
http://www.forces.org/evidence/carol/carol40.htm
Tex
Though statistics confuse me in studies like this, and perhaps that's where my confusion is coming from. What are the stats really saying, since I could twist those stats around and say that the larger percentage of folks with MC never took NSAIDs. But given my brain fog right now I'm not wrapping my brain around this correctly.
Well, hopefully the dr who told you to take the acid reducer for acid reflux actually tested your acid levels before tell you to take them. Perhaps you are producing too much acid.Mars wrote:Two comments:
#1 - I smoke and have for over 25 years - I have MC
#2 - the acid production - I'm confused - I take Nexium due to EXTREME acid reflux - if we are discussing that we produce "not enough acid", what's the deal with the reflux? Help me please!
Thanks
Mars
Actually that's not contrary, that fits in with what was found. They found that those who had smoked and quit were more likely to get LC than they were to get CC.starfire wrote:Well, I'm running contrary to the pack again. I smoked for 40 years. I got MC after I stopped smoking and my diagnosis was LC not CC.
I'm not trying to be contrary, just pointing out the differences. I enjoy all the research you all do.
Love, Shirley
Ah, I see what I'm missing for the statistics. The control group for smoking. Any of those studies have that? I see the ones for NSAIDs so obviously NSAIDs are one of the culprets. Though here's one problem, just be cause there is an incedence of NSAID use doesn't mean it's causative, though I would venture to guess that NSAID use is.
Who knows maybe those who develop MC are more likely to have pain that requires the use of NSAIDs because of something else.
Take this as an example, I'm fairly certain it's not true but bare with me. Let's say that some study shows that folks with MC were more likely to eat salty foods, ok. So salty foods are bad, we should avoid them. Right? Well, what if the problem wasn't the salty foods, but that folks who develop MC have less sodium in their body and thus craved salty foods and ate them. In this later case it was actually the missing/low salt that was the problem which would never get addressed.
Mike
Who knows maybe those who develop MC are more likely to have pain that requires the use of NSAIDs because of something else.
Take this as an example, I'm fairly certain it's not true but bare with me. Let's say that some study shows that folks with MC were more likely to eat salty foods, ok. So salty foods are bad, we should avoid them. Right? Well, what if the problem wasn't the salty foods, but that folks who develop MC have less sodium in their body and thus craved salty foods and ate them. In this later case it was actually the missing/low salt that was the problem which would never get addressed.
Mike
Mike,
I hear you. All these studies we're talking about are fairly old, (yours was from 1999, for example, and mine were dated even earlier), so a lot of water has gone under the bridge since then, (especially since researchers have only been aware of MC for roughly 20 years, so fully a third of that time has passed after those reports were published).
Yep, all sorts of claims can be made from the results of such studies, and the relevance of such claims is best determined by the reader, and possibly digested with a grain of salt. From the first link that you cited, for example:
Without that strict regimen of testing, any "ordering" of diagnoses, is an arbitrary process that depends upon the "luck of draw", so to speak. IOW, it depends on when the respective patients sought medical help in the first place, and what sequence of tests, (and under what time schedule), the GI doc decided to use for each particular patient, (the busier a doctor is, the longer time between the scheduling of tests, normally - it took my GI over two and a half months to get around to a colonoscopy). Logistically, there are far too many arbitrary events in this process to place any significant credence on the average interval of diagnosis. Besides the arbitrary nature of obtaining the biopsy samples in the first place, my guess is that part of the difference is simply due to the fact that lymphocytic infiltration is a much more obvious marker than thickened collagen layers, so LC is more likely to be diagnosed than CC, (unless the pathologist has sufficient time to devote to a thorough analysis).
Part of my reasoning here is a hunch that some busy pathologists may not feel the need to look any further, once lymphocytic infiltration has been documented. Afer all, additional time spent on that slide will not significantly affect the diagosis - the treatment is the same for any form of MC, and there is probably a stack of other cases waiting to be analyzed, (for life-threatening diseases, such as cancer), that are almost certainly viewed as more urgent.
I agree that statistics can be extremely confusing and misleading. Consider this, as a macroscopic analysis of the connection between smoking and MC:
In 2004, 22% of the U. S. population were officially classified as smokers. The "official" number of patients diagnosed with MC, was somewhere in the area of maybe 10 per 100,000 in the general population. This amounts to a prevalence of 0.0001, or 0.01%. 0.01 is only 0.045% of 22. That means that 99.95% of smokers did not have MC. When you look at it in that light, the connection is not very significant, is it?
To be honest, I think we're all confused, but we're aware of it, and the researchers are not. LOL.
Tex
P S Almost forgot - yes, using their statistics, it appears that people who stop smoking are more likely to be diagnosed with LC than CC, but how important is that observation, in light of the fact that it doesn't say a thing about the actual probability of smokers developing LC, CC, MC, or anything else? For all practical purposes, it's an irrelevant observation.
I hear you. All these studies we're talking about are fairly old, (yours was from 1999, for example, and mine were dated even earlier), so a lot of water has gone under the bridge since then, (especially since researchers have only been aware of MC for roughly 20 years, so fully a third of that time has passed after those reports were published).
Yep, all sorts of claims can be made from the results of such studies, and the relevance of such claims is best determined by the reader, and possibly digested with a grain of salt. From the first link that you cited, for example:
Note their claim, (which I have emphasized in red), that LC presents earlier than CC. I view that as an irrelevant observation, simply because there is nothing in the report to substantiate it. For that to be true, the doctors in each and every case would have had to document the progress of each of the patients, by taking biopsies immediately upon the onset of symptoms, and then they would have had to continue to take biopsies at frequent intervals, until the markers of either LC or CC were evident to the pathologists reviewing the slides. You and I both know that they did not do that.Mean duration of symptoms before diagnosis was two months for lymphocytic colitis and four months for collagenous colitis. Overall prognosis was generally mild; 84% of patients with lymphocytic colitis and 74% of patients with collagenous colitis reported resolution or significant improvement (p=0.033). CONCLUSIONS: Collagenous and lymphocytic colitis are similar but not identical. Patients with lymphocytic colitis present somewhat earlier and are less likely to be active smokers. Symptoms are milder and more likely to disappear in lymphocytic colitis.
Without that strict regimen of testing, any "ordering" of diagnoses, is an arbitrary process that depends upon the "luck of draw", so to speak. IOW, it depends on when the respective patients sought medical help in the first place, and what sequence of tests, (and under what time schedule), the GI doc decided to use for each particular patient, (the busier a doctor is, the longer time between the scheduling of tests, normally - it took my GI over two and a half months to get around to a colonoscopy). Logistically, there are far too many arbitrary events in this process to place any significant credence on the average interval of diagnosis. Besides the arbitrary nature of obtaining the biopsy samples in the first place, my guess is that part of the difference is simply due to the fact that lymphocytic infiltration is a much more obvious marker than thickened collagen layers, so LC is more likely to be diagnosed than CC, (unless the pathologist has sufficient time to devote to a thorough analysis).
Part of my reasoning here is a hunch that some busy pathologists may not feel the need to look any further, once lymphocytic infiltration has been documented. Afer all, additional time spent on that slide will not significantly affect the diagosis - the treatment is the same for any form of MC, and there is probably a stack of other cases waiting to be analyzed, (for life-threatening diseases, such as cancer), that are almost certainly viewed as more urgent.
I agree that statistics can be extremely confusing and misleading. Consider this, as a macroscopic analysis of the connection between smoking and MC:
In 2004, 22% of the U. S. population were officially classified as smokers. The "official" number of patients diagnosed with MC, was somewhere in the area of maybe 10 per 100,000 in the general population. This amounts to a prevalence of 0.0001, or 0.01%. 0.01 is only 0.045% of 22. That means that 99.95% of smokers did not have MC. When you look at it in that light, the connection is not very significant, is it?
To be honest, I think we're all confused, but we're aware of it, and the researchers are not. LOL.
Tex
P S Almost forgot - yes, using their statistics, it appears that people who stop smoking are more likely to be diagnosed with LC than CC, but how important is that observation, in light of the fact that it doesn't say a thing about the actual probability of smokers developing LC, CC, MC, or anything else? For all practical purposes, it's an irrelevant observation.