Writings on SIBO, Sugar Malabsorption and Leaky Gut
Moderators: Rosie, Stanz, Jean, CAMary, moremuscle, JFR, Dee, xet, Peggy, Matthew, Gabes-Apg, grannyh, Gloria, Mars, starfire, Polly, Joefnh
Writings on SIBO, Sugar Malabsorption and Leaky Gut
These are VERY ROUGH starts of what I plan to write. I'm thinking my last bit of issue is related to SIBO, though I am trying to figure out the cause of that (could be low acid production or motility issues).
Small Intestinal Bacterial Overgrowth (SIBO)
SIBO
Symptoms:
Weight loss
macrocytic anemia
Malabsorption
Depression/Anxiety (Tryptophan)
diarrhea, steatorrhea
protein-losing enteropathy
Causes:
1) Obstructed or reduced bile flow
2) Sugery of GI (stomach)
3) disturbance of gastrointestinal motility - movement of food through gut (paraplegia caused by spinal cord injury *a, Portal hypertension *b, chronic renal failure *c, diabetes and/or Autonomic neuropathy *d, Celiac Disease *e)
4) Low PH/Acid (due to physical reasons [Hypochlorhydria] or acid blocking/lowering medication) can cause b12 deficiency
5) systemic sclerosis
NOT CAUSES:
Loss of ileocecal valve
"Interestingly, loss of the ileocecal valve was not associated with an increased risk of bacterial overgrowth."
http://www.ncbi.nlm.nih.gov/entrez/quer ... med_docsum
TREATMENTS:
1) Administration of bile acids, activation of the bile acid receptor FXR
2) Most likely depends on what surgery was done.
Possible treatments I need to research:
Pepermint
Grapefruit Seed Extract
Acidic foods
Antibiotics
Cayenne Pepper (Capsicum frutescens)
Apple cider vinegar or lemon juice
Garlic?
Oregon Grape extract?
1) Regulation of antibacterial defense in the small intestine by the nuclear bile acid receptor.
http://www.ncbi.nlm.nih.gov/entrez/quer ... med_DocSum
2) Long-term consequences of total gastrectomy: quality of life, nutritional status, bacterial overgrowth and adaptive changes in esophagojejunostomic mucosa.
http://www.ncbi.nlm.nih.gov/entrez/quer ... med_DocSum
3a) Study of bacterial translocation from gut after paraplegia caused by spinal cord injury in rats.
http://www.ncbi.nlm.nih.gov/entrez/quer ... med_DocSum
3b) Small intestinal motility disturbances and bacterial overgrowth in patients with liver cirrhosis and portal hypertension.
http://www.ncbi.nlm.nih.gov/entrez/quer ... med_DocSum
3c) Patients with chronic renal failure have abnormal small intestinal motility and a high prevalence of small intestinal bacterial overgrowth.
http://www.ncbi.nlm.nih.gov/entrez/quer ... s=12853724
3d) Small-bowel bacterial overgrowth in diabetic subjects is associated with cardiovascular autonomic neuropathy.
http://www.ncbi.nlm.nih.gov/entrez/quer ... med_DocSum
Chronic diarrhoea and diabetes mellitus: prevalence of small intestinal bacterial overgrowth.
http://www.ncbi.nlm.nih.gov/entrez/quer ... med_DocSum
3e) Gluten sensitivity as a neurological illness
http://jnnp.bmjjournals.com/cgi/content ... f_ipsecsha
4) Suppression of gastric acid secretion in patients with gastroesophageal reflux disease results in gastric bacterial overgrowth and deconjugation of bile acids.
http://www.ncbi.nlm.nih.gov/entrez/quer ... med_DocSum
5) Digestive manifestations in systemic sclerosis
http://www.ncbi.nlm.nih.gov/entrez/quer ... s=12218892
SIBO
Symptoms:
Weight loss
macrocytic anemia
Malabsorption
Depression/Anxiety (Tryptophan)
diarrhea, steatorrhea
protein-losing enteropathy
Causes:
1) Obstructed or reduced bile flow
2) Sugery of GI (stomach)
3) disturbance of gastrointestinal motility - movement of food through gut (paraplegia caused by spinal cord injury *a, Portal hypertension *b, chronic renal failure *c, diabetes and/or Autonomic neuropathy *d, Celiac Disease *e)
4) Low PH/Acid (due to physical reasons [Hypochlorhydria] or acid blocking/lowering medication) can cause b12 deficiency
5) systemic sclerosis
NOT CAUSES:
Loss of ileocecal valve
"Interestingly, loss of the ileocecal valve was not associated with an increased risk of bacterial overgrowth."
http://www.ncbi.nlm.nih.gov/entrez/quer ... med_docsum
TREATMENTS:
1) Administration of bile acids, activation of the bile acid receptor FXR
2) Most likely depends on what surgery was done.
Possible treatments I need to research:
Pepermint
Grapefruit Seed Extract
Acidic foods
Antibiotics
Cayenne Pepper (Capsicum frutescens)
Apple cider vinegar or lemon juice
Garlic?
Oregon Grape extract?
1) Regulation of antibacterial defense in the small intestine by the nuclear bile acid receptor.
http://www.ncbi.nlm.nih.gov/entrez/quer ... med_DocSum
2) Long-term consequences of total gastrectomy: quality of life, nutritional status, bacterial overgrowth and adaptive changes in esophagojejunostomic mucosa.
http://www.ncbi.nlm.nih.gov/entrez/quer ... med_DocSum
3a) Study of bacterial translocation from gut after paraplegia caused by spinal cord injury in rats.
http://www.ncbi.nlm.nih.gov/entrez/quer ... med_DocSum
3b) Small intestinal motility disturbances and bacterial overgrowth in patients with liver cirrhosis and portal hypertension.
http://www.ncbi.nlm.nih.gov/entrez/quer ... med_DocSum
3c) Patients with chronic renal failure have abnormal small intestinal motility and a high prevalence of small intestinal bacterial overgrowth.
http://www.ncbi.nlm.nih.gov/entrez/quer ... s=12853724
3d) Small-bowel bacterial overgrowth in diabetic subjects is associated with cardiovascular autonomic neuropathy.
http://www.ncbi.nlm.nih.gov/entrez/quer ... med_DocSum
Chronic diarrhoea and diabetes mellitus: prevalence of small intestinal bacterial overgrowth.
http://www.ncbi.nlm.nih.gov/entrez/quer ... med_DocSum
3e) Gluten sensitivity as a neurological illness
http://jnnp.bmjjournals.com/cgi/content ... f_ipsecsha
4) Suppression of gastric acid secretion in patients with gastroesophageal reflux disease results in gastric bacterial overgrowth and deconjugation of bile acids.
http://www.ncbi.nlm.nih.gov/entrez/quer ... med_DocSum
5) Digestive manifestations in systemic sclerosis
http://www.ncbi.nlm.nih.gov/entrez/quer ... s=12218892
Sugar Malabsorption
Symptoms:
Diarrhea
Gas
Cramping/Pain
Loss of Energy
Malabsorption of other foods/vitamins/minerals
Anemia
Depression/Anxiety
Malabsorbtion (for all types of sugars)
Food goes through small intestine too quickly
Small Intestinal Bacterial Overgrowth (SIBO)
Monosaccharides
glucose (dextrose)
Readily absorbed by the body
Fructose
Requires some work to absorb
Malabsorption
due to defficency of aldolase B to absorb it
Not enough glucose to help absorb it
galactose
Mostly derived from lactose, but can be found in sugar beets.
ribose
Not sure where it comes from
Part of DNA
Disaccharides
Maltose
glucose + glucose
Malabsorbtion
Missing Maltase enzyme (produced in villi)
Not enough stomac acid ?
Lactose
glucose + galactose
Malabsorbtion
Missing Lactase enzyme (produced in villi)
Sucrose
glucose + fructose
Malabsorbtion
due to malabsorbtion of sugars broken down into
Not enough stomac acid ?
Missing enzymes sucrase (produced in villi) or isomaltase
Polysaccharides
Starches
glucose polymers
Needs Amylase produced in pancreatic juice and saliva
Broken down into maltose
Glycogen
polymer of glucose
Cellulose
repeated glucose units bonded together
Not broken down by body but can be by bacteria
TESTING
Lactulose/mannitol Breath Test
D-xylose
Glucose
Low Tryptophan, Niacin, Seratonin
Symptoms:
Diarrhea
Gas
Cramping/Pain
Loss of Energy
Malabsorption of other foods/vitamins/minerals
Anemia
Depression/Anxiety
Malabsorbtion (for all types of sugars)
Food goes through small intestine too quickly
Small Intestinal Bacterial Overgrowth (SIBO)
Monosaccharides
glucose (dextrose)
Readily absorbed by the body
Fructose
Requires some work to absorb
Malabsorption
due to defficency of aldolase B to absorb it
Not enough glucose to help absorb it
galactose
Mostly derived from lactose, but can be found in sugar beets.
ribose
Not sure where it comes from
Part of DNA
Disaccharides
Maltose
glucose + glucose
Malabsorbtion
Missing Maltase enzyme (produced in villi)
Not enough stomac acid ?
Lactose
glucose + galactose
Malabsorbtion
Missing Lactase enzyme (produced in villi)
Sucrose
glucose + fructose
Malabsorbtion
due to malabsorbtion of sugars broken down into
Not enough stomac acid ?
Missing enzymes sucrase (produced in villi) or isomaltase
Polysaccharides
Starches
glucose polymers
Needs Amylase produced in pancreatic juice and saliva
Broken down into maltose
Glycogen
polymer of glucose
Cellulose
repeated glucose units bonded together
Not broken down by body but can be by bacteria
TESTING
Lactulose/mannitol Breath Test
D-xylose
Glucose
Low Tryptophan, Niacin, Seratonin
Leaky Gut
Leads to Leaky Gut
Stress, COX inhibition (NSAIDs), Bateria "bad", Virus, gliadin (gluten/wheat), sucrose monoester fatty acids (Olestra), Ethanol (Alcohol), Yeast, oxidative stress
Stress stimulates transepithelial macromolecular uptake in rat jejunum
http://ajpgi.physiology.org/cgi/content ... 75/5/G1037
COX inhibition excites enteric nerves that affect motility, alkaline secretion, and permeability in rat duodenum
http://ajpgi.physiology.org/cgi/content ... 81/5/G1169
Surfactants enhance the tight-junction permeability of food allergens in human intestinal epithelial Caco-2 cells.
http://www.ncbi.nlm.nih.gov/entrez/quer ... med_DocSum
Ethanol modulation of intestinal epithelial tight junction barrier.
http://www.ncbi.nlm.nih.gov/entrez/quer ... s=10198341
Disruption of Epithelial Tight Junctions by Yeast Enhances the Paracellular Delivery of a Model Protein.
http://www.ncbi.nlm.nih.gov/entrez/quer ... med_DocSum
Tyrosine phosphorylation and dissociation of occludin-ZO-1 and E-cadherin-beta-catenin complexes from the cytoskeleton by oxidative stress.
http://www.ncbi.nlm.nih.gov/entrez/quer ... s=12169098
Turning back leaky gut
GLP2, Good bacteria, Calicium?, Glutamine
Glutamine regulates Caco-2 cell tight junction proteins.
http://www.ncbi.nlm.nih.gov/entrez/quer ... med_docsum
Mechanism of extracellular calcium regulation of intestinal epithelial tight junction permeability: role of cytoskeletal involvement.
http://www.ncbi.nlm.nih.gov/entrez/quer ... s=11054866
Glucagon-like peptide-2-enhanced barrier function reduces pathophysiology in a model of food allergy
http://ajpgi.physiology.org/cgi/content ... 284/6/G905
Circulating and tissue forms of the intestinal growth factor, glucagon-like peptide-2.
http://www.ncbi.nlm.nih.gov/entrez/quer ... t=Abstract
Plasma concentrations of glucagon-like peptide-2 in adult patients with treated and untreated coeliac disease.
http://www.ncbi.nlm.nih.gov/entrez/quer ... med_DocSum
Leads to Leaky Gut
Stress, COX inhibition (NSAIDs), Bateria "bad", Virus, gliadin (gluten/wheat), sucrose monoester fatty acids (Olestra), Ethanol (Alcohol), Yeast, oxidative stress
Stress stimulates transepithelial macromolecular uptake in rat jejunum
http://ajpgi.physiology.org/cgi/content ... 75/5/G1037
COX inhibition excites enteric nerves that affect motility, alkaline secretion, and permeability in rat duodenum
http://ajpgi.physiology.org/cgi/content ... 81/5/G1169
Surfactants enhance the tight-junction permeability of food allergens in human intestinal epithelial Caco-2 cells.
http://www.ncbi.nlm.nih.gov/entrez/quer ... med_DocSum
Ethanol modulation of intestinal epithelial tight junction barrier.
http://www.ncbi.nlm.nih.gov/entrez/quer ... s=10198341
Disruption of Epithelial Tight Junctions by Yeast Enhances the Paracellular Delivery of a Model Protein.
http://www.ncbi.nlm.nih.gov/entrez/quer ... med_DocSum
Tyrosine phosphorylation and dissociation of occludin-ZO-1 and E-cadherin-beta-catenin complexes from the cytoskeleton by oxidative stress.
http://www.ncbi.nlm.nih.gov/entrez/quer ... s=12169098
Turning back leaky gut
GLP2, Good bacteria, Calicium?, Glutamine
Glutamine regulates Caco-2 cell tight junction proteins.
http://www.ncbi.nlm.nih.gov/entrez/quer ... med_docsum
Mechanism of extracellular calcium regulation of intestinal epithelial tight junction permeability: role of cytoskeletal involvement.
http://www.ncbi.nlm.nih.gov/entrez/quer ... s=11054866
Glucagon-like peptide-2-enhanced barrier function reduces pathophysiology in a model of food allergy
http://ajpgi.physiology.org/cgi/content ... 284/6/G905
Circulating and tissue forms of the intestinal growth factor, glucagon-like peptide-2.
http://www.ncbi.nlm.nih.gov/entrez/quer ... t=Abstract
Plasma concentrations of glucagon-like peptide-2 in adult patients with treated and untreated coeliac disease.
http://www.ncbi.nlm.nih.gov/entrez/quer ... med_DocSum
Mike!
I didn't realize you were going to write up all of this research you have been doing. That's FANTASTIC! When you are finished, let's be sure to put it in one of the forums for reference so it doesn't get lost.
Love,
Polly
I didn't realize you were going to write up all of this research you have been doing. That's FANTASTIC! When you are finished, let's be sure to put it in one of the forums for reference so it doesn't get lost.
Love,
Polly
Blessed are they who can laugh at themselves, for they shall never cease to be amused.
I sure will. They need a lot of work yet, but I'm finding this all pretty interesting.Polly wrote:Mike!
I didn't realize you were going to write up all of this research you have been doing. That's FANTASTIC! When you are finished, let's be sure to put it in one of the forums for reference so it doesn't get lost.
Love,
Polly
FYI here's my theory on MC.
I think that gluten/MC are connected. Here's one possible way that I've been thinking about.
Gluten (gliadin specfically) causes (even in normal folks) the tight junctions in the gut to open. This is proven. By the way there are a bunch of other ways that the tight junctions are opened, I mention a few in the other thread I started on the research I did. What's "wonderful" about some of these are that some are recent man made additions to our diet or treatments for symptoms (and not diseases).
Once these tight junctions open far enough proteins can make their way into the gut and we build antibodies for those proteins. Also proven.
Let's just say that we all had Small Intestinal Bacterial Overgrowth. Can't prove, but given that something like 84% of folks diagnosed with IBS had SIBO or at least tests pointed towards this and that 74% improved symptoms when treated for SIBO I wouldn't think this would be a stretch.
So, the good and bad bacteria (which is normally in the colon but in SIBO is in the small intestines) make it's way through the open tight junctions and we develop antibodies for said bacteria where before it was tollerated. This can be proven in that this is how pathogens are eliminated by the immune system.
Well, now all bets are off, the bacteria even in the colon are "attacked" and then we get all sorts of wonderful symptoms or even other diseases.
Mike
Forgot to add, that this would explain spontaneous remission in some and continuing problems in others.
It helps to explain why some antibiotics helped, but didn't cure. Why a lot of us have problems with proteins. Why a lot of us have issues with sugars. This would also explain why some can eat gluten whereas others cannot.
If this is all true then I think we have to do the following to end it. We've got to first stop having a leaky gut, without this it will never be fixed. Another related item is to make sure that we don't have SIBO.
Then (and this is the unknown for me) we have to stop developing the antibodies for what ever bacteria we are developing it for. At least the normal gut flora.
What lead me here is this:
http://www.ncbi.nlm.nih.gov/entrez/quer ... med_docsum
What is interesting here is the mention of IL-15. This is involved in memory of pathogens. Our guts seem to remember an attack, I'm guessing the first attack. So until our immune system forgets, or doesn't see the pathgens we continue to have problems.
It helps to explain why some antibiotics helped, but didn't cure. Why a lot of us have problems with proteins. Why a lot of us have issues with sugars. This would also explain why some can eat gluten whereas others cannot.
If this is all true then I think we have to do the following to end it. We've got to first stop having a leaky gut, without this it will never be fixed. Another related item is to make sure that we don't have SIBO.
Then (and this is the unknown for me) we have to stop developing the antibodies for what ever bacteria we are developing it for. At least the normal gut flora.
What lead me here is this:
http://www.ncbi.nlm.nih.gov/entrez/quer ... med_docsum
What is interesting here is the mention of IL-15. This is involved in memory of pathogens. Our guts seem to remember an attack, I'm guessing the first attack. So until our immune system forgets, or doesn't see the pathgens we continue to have problems.
Hi Mike,
This sure is interesting. There seem to be many things that can open those gut "gates". I'm also thinking of lectins in foods other than grain (legumes for example) and zonulin, which the body apparently makes naturally. I can't remember if you've seen Dr. Fasano's research on zonulin, but here is a summary:
The following is a summary of an article that appeared in the University of Maryland Medical Alumni Association "Bulletin" in spring, 2005, volume 89, No. 4.
Dr. Alessio Fasano, a world's foremost researcher of celiac disease, has found a way to prevent type I diabetes (an autoimmune disease) in rats who are genetically prone to develop the disease. This discovery could lead to the prevention/treatment of other autoimmune diseases too, like celiac disease or rheumatoid arthritis or maybe even MC!
The way in which the study prevented the onset of type I diabetes was by CHANGING THE PERMEABILITY OF THE INTESTINAL WALL. Earlier research by Dr. Fasano and team had led to the discovery of a human protein called "zonulin". It was found that zonulin regulates the permeability of the intestine by controlling the opening and closing of specialized structures that act like gates between cells. When the body produces too much zonulin, these gates get stuck open for too long and allow undigested foodstuff, toxins, and bacterial/viral particles to enter the immune system. This leads to the production of antibodies. These antibodies can then destroy the insulin-producing cells in the pancreas of folks genetically prone to develop type I diabetes, as well as destroy other organs/tissues affected by autoimmune disease.
Dr. Fasano found that zonulin is produced in very large amounts in people who suffer from autoimmune disorders such as type I diabetes, celiac disease, multiple sclerosis, and rheumatoid arthritis. According to him, "these diseases are all characterized by an extremely permeable intestinal wall". With funding from the NIH, Dr. Fasano has developed a zonulin inhibitor peptide, called AT-1001, which prevents zonulin from regulating intestinal permeability. This peptide prevented the development of disease in the vast majority (73%) of the rats tested.
The research team is currently developing an oral medication containing AT-1001 and has plans to start clinical trials on humans with celiac disease as soon as FDA approval is granted. To think that an oral medication might be able to arrest autoimmune diseases in the early stages......WOW!
SO, what do you think is the common denominator for all of these things that can open the gates? Maybe the lectins or SIBO or NSAIDs (or whatever) somehow urge the body to make zonulin. If that is the case, then maybe the anti-zonulin peptide Dr. Fasano has developed will close the gates no matter what causes them to open? Now that would be lovely, wouldn't it?
Love,
Polly
This sure is interesting. There seem to be many things that can open those gut "gates". I'm also thinking of lectins in foods other than grain (legumes for example) and zonulin, which the body apparently makes naturally. I can't remember if you've seen Dr. Fasano's research on zonulin, but here is a summary:
The following is a summary of an article that appeared in the University of Maryland Medical Alumni Association "Bulletin" in spring, 2005, volume 89, No. 4.
Dr. Alessio Fasano, a world's foremost researcher of celiac disease, has found a way to prevent type I diabetes (an autoimmune disease) in rats who are genetically prone to develop the disease. This discovery could lead to the prevention/treatment of other autoimmune diseases too, like celiac disease or rheumatoid arthritis or maybe even MC!
The way in which the study prevented the onset of type I diabetes was by CHANGING THE PERMEABILITY OF THE INTESTINAL WALL. Earlier research by Dr. Fasano and team had led to the discovery of a human protein called "zonulin". It was found that zonulin regulates the permeability of the intestine by controlling the opening and closing of specialized structures that act like gates between cells. When the body produces too much zonulin, these gates get stuck open for too long and allow undigested foodstuff, toxins, and bacterial/viral particles to enter the immune system. This leads to the production of antibodies. These antibodies can then destroy the insulin-producing cells in the pancreas of folks genetically prone to develop type I diabetes, as well as destroy other organs/tissues affected by autoimmune disease.
Dr. Fasano found that zonulin is produced in very large amounts in people who suffer from autoimmune disorders such as type I diabetes, celiac disease, multiple sclerosis, and rheumatoid arthritis. According to him, "these diseases are all characterized by an extremely permeable intestinal wall". With funding from the NIH, Dr. Fasano has developed a zonulin inhibitor peptide, called AT-1001, which prevents zonulin from regulating intestinal permeability. This peptide prevented the development of disease in the vast majority (73%) of the rats tested.
The research team is currently developing an oral medication containing AT-1001 and has plans to start clinical trials on humans with celiac disease as soon as FDA approval is granted. To think that an oral medication might be able to arrest autoimmune diseases in the early stages......WOW!
SO, what do you think is the common denominator for all of these things that can open the gates? Maybe the lectins or SIBO or NSAIDs (or whatever) somehow urge the body to make zonulin. If that is the case, then maybe the anti-zonulin peptide Dr. Fasano has developed will close the gates no matter what causes them to open? Now that would be lovely, wouldn't it?
Love,
Polly
Blessed are they who can laugh at themselves, for they shall never cease to be amused.
Yep, Zonulin is the mechanism in a few of the ones I mentioned, specfically gluten, but also in others as well I suspect.Polly wrote:Hi Mike,
This sure is interesting. There seem to be many things that can open those gut "gates". I'm also thinking of lectins in foods other than grain (legumes for example) and zonulin, which the body apparently makes naturally. I can't remember if you've seen Dr. Fasano's research on zonulin, but here is a summary:
SO, what do you think is the common denominator for all of these things that can open the gates? Maybe the lectins or SIBO or NSAIDs (or whatever) somehow urge the body to make zonulin. If that is the case, then maybe the anti-zonulin peptide Dr. Fasano has developed will close the gates no matter what causes them to open? Now that would be lovely, wouldn't it?
Love,
Polly
I'd say the most common would be NSAIDs, and guess who it appears to have related GI diseases more and who pops NSAIDs during certain times of the month and who also is more susceptable to autoimmune diseases. :( Women. Yikes!
Perhaps with the invetion of Olestra (and them hiding it in foods and not labeling them) I'm afraid we're going to see younger and younger folks who might be eating this products in foods who get these types of diseases.
And on the anti-zonulin peptide... I'm not so sure this is a good idea. Those gates need to open for reasons that your body needs so closing them is again... a treatment for a symptom. :( I'm definitly interested in the research done to find this anti peptide, but I'm concerned about what it might bring. If they can figure out a way to use this and still have the body do what it needs to do then I'm all for it, otherwise we're messing with something that shouldn't be. In my opinion.
Mike
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Wow,
That's alot of research you have done Mike. THANK YOU!
Love,
Joanna
That's alot of research you have done Mike. THANK YOU!
Love,
Joanna
THE GLUTEN FILES
http://jccglutenfree.googlepages.com/
http://jccglutenfree.googlepages.com/
Hi Mike,
FWIW, when my test for bacterial overgrowth came back with an overgrowth of both good and bad bacteria, they also tested the bacteria for what would kill them. Along with cipro and a few other antibiotics, caprylic acid and Uva Ursi were supposed to be effective in killing them. After my fun with the acid pills and the probiotics, I've been too chicken to experiment again. But if you are right about the SIBO and the leaky gut connection...maybe I'll get brave and try the caprylic acid pills as it's something that I could continue to take..unlike an antibiotic. I'll let you know when or if I get brave. Thanks for all your research.
Love, Cristi
FWIW, when my test for bacterial overgrowth came back with an overgrowth of both good and bad bacteria, they also tested the bacteria for what would kill them. Along with cipro and a few other antibiotics, caprylic acid and Uva Ursi were supposed to be effective in killing them. After my fun with the acid pills and the probiotics, I've been too chicken to experiment again. But if you are right about the SIBO and the leaky gut connection...maybe I'll get brave and try the caprylic acid pills as it's something that I could continue to take..unlike an antibiotic. I'll let you know when or if I get brave. Thanks for all your research.
Love, Cristi
Just thinking out loud here...........if the SIBO is caused by the same bacteria that is present in the colon (large intestine), how would treatment preferentially kill off the bacteria in the SI and not the colon?
Cristi, please tell us more about caprylic acid and Uva Ursi.
Love,
Polly
Cristi, please tell us more about caprylic acid and Uva Ursi.
Love,
Polly
Blessed are they who can laugh at themselves, for they shall never cease to be amused.
Hi Mike,
You've been busy, to say the least.
In your second post, you had the line:
I hope you don't mind, but I took the liberty of editing that line, by ending the paragraph, (hitting the "Enter" key), after the ".", and before the http, so that the system can now properly identify and handle the URL, and horizontal scrolling is no longer necessary, and so that the left edge of the URL lines up with the rest of them.
If this isn't the way that the line is supposed to read, please let me know, and I will change it, since I certainly didn't intend to change something that shouldn't be changed.
Tex
You've been busy, to say the least.
In your second post, you had the line:
I have modified the code for the system, so that it recognizes "long" URLs, and automatically shortens them, (without losing the navigation links), in order to eliminate the need for horizontal scrolling, (horizontal scrolling takes most of the fun out of readig a topic with a long URL). The way it was written, the "mucosa." in front of the "http" in that line, prevented the system from shortening the URL, and also prevented it from turning it into a link. Instead, the system just intrpreted it as one long word, thus the reason that horizontal scrolling was necessary to read this topic.mucosa.http://www.ncbi.nlm.nih.gov/entrez/quer ... stractPlus . . . . . .
I hope you don't mind, but I took the liberty of editing that line, by ending the paragraph, (hitting the "Enter" key), after the ".", and before the http, so that the system can now properly identify and handle the URL, and horizontal scrolling is no longer necessary, and so that the left edge of the URL lines up with the rest of them.
If this isn't the way that the line is supposed to read, please let me know, and I will change it, since I certainly didn't intend to change something that shouldn't be changed.
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 Cristi, did they say what bacteria they found?cludwig wrote:Hi Mike,
FWIW, when my test for bacterial overgrowth came back with an overgrowth of both good and bad bacteria, they also tested the bacteria for what would kill them. Along with cipro and a few other antibiotics, caprylic acid and Uva Ursi were supposed to be effective in killing them. After my fun with the acid pills and the probiotics, I've been too chicken to experiment again. But if you are right about the SIBO and the leaky gut connection...maybe I'll get brave and try the caprylic acid pills as it's something that I could continue to take..unlike an antibiotic. I'll let you know when or if I get brave. Thanks for all your research.
Love, Cristi
Also, what reaction did you have to the acid pills? I was told to try some HCL Acid pills as I think my acid production is too low. It may have been coincidence, but the day after I had terrible D. :(
Did they test you for acid production or just assume?
Thanks,
Mike
It cannot. :( At least as far as I know. Perhaps some day down the road they could come up with antibiotics or some other treatments that are preferential.Polly wrote:Just thinking out loud here...........if the SIBO is caused by the same bacteria that is present in the colon (large intestine), how would treatment preferentially kill off the bacteria in the SI and not the colon?
Cristi, please tell us more about caprylic acid and Uva Ursi.
Love,
Polly
Supposedly there are some natural remedies that may target only the bad bacteria. I'll have to get that info again as I forgot. One of them may be part of Peppermint.
Mike