FYILACTOSE INTOLERANCE AND SMALL BOWEL BACTERIAL OVERGROWTH IN IRRITABLE BOWEL SYNDROMEhttp://ibsgroup.org/groupee/forums?a=tpc&s...06862#412106862
LI and SIBO Info
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If fructose intolerance is as widespread as Thiwan and Pimentel claim, then Gottschall's theory is blown to smithereens. She claims that monosaccharides, including fructose, require no digestion before being absorbed in the small intestine.Pimentel, in his book (page 58), disputes Thiwan's claim in his final paragraph that cultures of jejunal fluid are required to make a conclusive determination with regard to SIBO. Pimentel claims that such cultures are unreliable because (a) we don't know how to culture many of the jejunal bacteria; (
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the instrument used to collect jejunal bacteria would be contaminated by bacteria from the mouth and other locations; and © jejunal bacteria would die when removed from the patient and exposed to oxygen.I am not qualified to judge the legitimacy of Pimentel's claims. But even I am aware of Koch's Postulates and certainly Pimentel is. I can't believe he is intentionally avoiding culturing jejunal bacteria because he wants to protect his theory from being tested empirically. If that is what he is doing then he deserves to have scorn heaped upon him. But that does not appear to be his modus operandi. In the past, when his experimental methods have been criticized, he has redesigned his experiments to address those criticisms, including some of the criticisms levelled by Thiwan.I think it is important that we all be conscious of the attacks directed at Pimentel and Eric is doing us all a service by making sure none of us lose sight of them. But the journal articles are not all that we need go on. This forum and the experiences of its members provide lots of raw, unsystematic, but in many cases prospective, data. I would encourage everyone here to log their experiences on the SIBO protocols, starting from before they begin the protocol. We can develop our own data set using the resources of this forum.
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Fructose doesn't require any digestion before being absorbed. Lactose does, Sucrose does, but fructose and glucose do not.Frutose intolerance is all about not being able to absorb it normally, not at all about breaking it down.Fructose is normally best absorbed when it is in a 1:1 ratio with glucose, but even that doesn't help everyone.K.
From "Dietary Fructose and Gastrointestinal Symptoms: A Review""Fructose is commonly used to sweeten processed foods, and the prevalence of incomplete fructose absorption (25 g, 10%) in healthy subjects is as high as 50%."So maybe Pimentel is right in being cautious?
Your correction is well-taken. I should have been clearer. Gottschall claims that fructose is benign because it is does not require digestion. I should have stated clearly that Gottschall assumes that that which requires no digestion will be absorbed. It is the bolded statement which is refuted by the evidence of high levels in the population of fructose intolerance.
Pimentel, after claiming that jejunal fluid cultures are unreliable, does mention that there have been studies culturing duodenal bacteria. He states that 12% of those with IBS had duobdenal bacterial infections and that those who tested positive for duodenal infection had the worst IBS symptoms. These findings are of interest to me because elsewhere Pimentel mentions that Vivonex has close to a 90% success rate. It would seem to me that Vivonex could not be successful if SIBO explained IBS and there was a duodenal bacterial overgrowth. According to SIBO theory, Vivonex works because nutrients are absorbed before they reach bacteria. So, most people have their bacterial overgrowth in the jejunum, hence Vivonex works by being absorbed above the jejunum. But Vivonex is absorbed in the duodenum, so Vivonex would not help someone with a duodenal infection.The numerical fit here is almost too perfect. Twelve percent of IBSers have a duodenal infection. And slightly less than 90% of IBSers are not helped by Vivonex.
Moises, Where does Pimental talk about duodenal bacterial overgrowth? I've been looking for information on this specifically, as I suspect that might be what my son has. Have you read anything about the protocol if the bacteria is in the duodenum? To google it gets me nowhere - results are all for duodenal ulcers. Thanks.
Page 59 cites a study by Simren and Robson. I believe you have stated that your son had some improvement after Vivonex. If there is merit to Pimentel's explanations, one might tell a story like the following: some people have bacteria in the ileum and jejunum only, others have it in the duodenum, jejunum, and ileum. Vivonex eradicates ileal and jejunal overgrowths but feeds duodenal overgrowths. Your son improved when his ileal and jejunal overgrowths were eradicated but some symptoms lingered and those are explained by the persistence of the duodenal overgrowth. Kathleen's forcing me to clarify Gottschall's claim that that which requires no digestion will be absorbed got me thinking. Pimentel, though he cautions us to minimize fructose intake, must subscribe to a similar thesis. That is why he claims that glucose breath tests provide no useful information: since glucose requires no digestion Pimentel claims it will be absorbed.The exact mechanisms of Pimentel's protocols are not totally clear to me. Does Pimentel believe he is sterilizing the entire gut or merely the small intestine? Since Pimentel's hypothesis is that bacteria that are safe in the colon are dangerous in the small intestine, one wonders why flatulence problems would be resolved when bacteria that exist in the colon are eradicated from the small intestine. One might assume, that a bacterium that causes flatulence in the small intestine would do so in the colon as well. Of course, that might be a faulty assumption. There might be something about the colonic environment besides bacteria (or the presence of additional bacterial species) which affects flatulence.
That's a very good question. Here's a tentative answer: the bacteria need food to produce gas. Bacteria in the small bowel have access to a great deal of undigested food. However, bacteria in the colon only have access to leftovers. So, the idea is to have as much carbs as possible fully digested before they hit the colon (and eliminate those pesky bacteria in the small bowel.)
One thing, "classic IBS" is considered a problem in the large intestings.Rectal Ballon testing viceral hypersensivity tests where there insert a ballon up the rectum and apply various pressure shows the majority of IBSers have lower pain thresholds to distension of the colon. also 80 percent of IBSers have rectal hypersensivity. At one time they thought it might be a marker.Antibiotcs kill all bacteria. The bacteria produce gases and even small amounts of gas bubbles put pressure on the colon, and the pressure activates the colon to distend. Until its distened there are no sensations.Without being distened you could basically cut the colon and a person would not feel it. SIBO is forcing all bacteria into the samll bowel where it should not be as its pretty sterile.Something else to note in preliminary probiotics studies is some relief from pain and bloating. So here they are adding good bacteria and its helping with pain and bloating somewhat, although that mechanism of action has not been figured out yet fully, especially for each strain.The sensivity of the colon is why stress, hormones and foods as well as bacteria in IBS can all bring on symptoms.IBS pateints have different mri and pet scans then to normals or those with IBD. This is very important research to understand how pain is being processed in the brain in IBS. All pain is processed there.There is also research in IBS of pain and non painful pathways, where nerves are reporting pain that they should not be.So in IBS research at least its not toally about the small bowel, like it might be for someone with just sibo.I think you all might find DR Spliiers work really interesting.For example a major researcher in Post infectious IBS and abnormalities in Chornic d and motility in IBS and some other conditions.Neurogastroenterol Motil. 2006 Dec;18(12):1045-1055. Role of motility in chronic diarrhoea.Spiller R.Wolfson Digestive Diseases Centre, University Hospital, Nottingham, UK.Patients complaining of 'chronic diarrhoea' usually mean the passage of loose, urgent stools. Chronic diarrhoea is a feature of malabsorption; it may also be seen in the 'dumping syndrome' which follows gastric surgery, small intestinal bacterial overgrowth, bile salt malabsorption and in malabsorption of simple sugars including most commonly lactose, fructose and sorbitol. Excessively rapid entry of chyme into the small or large intestine generates propulsive motor patterns leading to accelerated transit. Inflammation is associated with decreased normal mixing motor patterns but increased propulsive motility including high amplitude propagated contractions (HAPCs). Evidence for abnormal small intestinal motility in the diarrhoea associated with irritable bowel syndrome (IBS) is conflicting and any difference appears small. Increased colonic HAPCs with increased propulsion is seen in IBS with diarrhoea (IBS-D). Stress-induced colonic motility is increased in IBS-D with hyper-responsiveness to corticotrophin releasing factor (CRF). Long-lasting increases in mucosal serotonin availability may contribute to the chronic diarrhoea seen in IBS-D and coeliac disease. Treatments for abnormal motility in chronic diarrhoea include those designed to correct specific underlying abnormalities including octreotide, antibiotics, colestyramine, specific food avoidance and anti-inflammatory agents. There are also treatments aimed primarily at altering motility directly including opiates, 5HT3 receptor antagonists and amitriptyline.PMID: 17109687
Just fyiThis is important to all thisVisceral Sensations and Brain-Gut MechanismsBy: Emeran A. Mayer, M.D., Professor of Medicine, Physiology and Psychiatry; Director, Center for Neurovisceral Sciences & Women's Health, David Geffen School of Medicine at UCLAhttp://www.aboutibs.org/Publications/VisceralSensations.htmlAnother aspect is serotonin has to be involved as its the messenger for pain from the gut to the brain."Neuroimaging has provided evidence of physiological differences between normal individualsand those suffering from IBS in the way a visceral stimulus (ie, rectal distention) is processed inthe brain.[14,15] Initial data from positron emission tomography (PET) scans demonstratedincreased activation of the anterior cingulate cortex (ACC) among normal individuals, comparedto IBS patients. The ACC is a cerebral cortical area that is rich in opiate receptors and is thought to be a major component of cognitive circuits relating to perception as well as descending spinal pathways involving pain. More recently, fMRI was used to demonstrate increased activity in the ACC, prefrontal (PF), and insular cortex areas, and in the thalamus of IBS patients compared to normal individuals."
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also in regards to dthis is a normal and an IBSers 15 minutes after eating of the sigmoid colon
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and an IBSers
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and an altered gastro colonic responce in IBSThis has been known for some time now. The "act of eating" can trigger symptoms, by the stomach basically telling the lower colon foods on the way and to get rid of what it has and it over reacts and cause d.
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