Get My FREE Copy
The Five Must-Knows for Treating SIBO
that have helped every person I've worked with.


As published in Today’s Practitioner: My editorial response to May 21, 2019 Today’s Practitioner article, Improved Anxiety Symptoms Over Just Probiotic. The article highlights a study that looked for evidence linking reduced anxiety symptoms with regulation of intestinal microbiota. The article stated, “(it is)…the benefits of non-probiotic food and supplements, such as a dietary FODMAP, that makes this study unique.”

As the FODMAP diet grows in popularity, we need to be clear about what the research has revealed. There is a pervasive misunderstanding of what the FODMAP diet does and does not do, and how it should be used in a clinical setting.

The review study referenced in the article, Effects Of Regulating Intestinal Microbiota On Anxiety Symptoms: A Systematic Review, published in General Psychiatry, looked at twenty–one studies; fifteen of which were probiotic interventions and six were dietary interventions.  Eleven studies in all showed a positive reduction of anxiety symptoms. Five of these studies were probiotic interventions and six were non-probiotic interventions. Of the five studies that were non-probiotic interventions, there were only two studies that look directly at a low FODMAP diet (LFD). [1]

One single-blind prospective study compared a 4–week LFD to the mNICE diet (a validated diet used in the treatment of IBS-D) in 84 subjects, and the results showed that the LFD intervention outperformed the mNICE diet, improving quality of life and anxiety scores. [2]

The second study compared a 4 week low FODMAP diet against yoga, and although both groups showed improved anxiety scores, the yoga intervention showed the most improvements.[3]

Two of the non-probiotic intervention studies looked at the effects of galactooligosaccharide  (GOS) supplementation vs. resistant dextrin as the control. The fifth was labeled ‘nutrition intervention’ but neither the study, nor the specific interventions were made available for review.

When only two of the studies looked at a LFD and in one of the studies yoga was even more successful at reducing anxiety, should the FODMAP diet be singled out?

It is also clear that the author of the review study cited in the article in question is correlating a reduction in anxiety symptoms solely to the catch-all mechanism “regulation of intestinal microbiota.”

To say that probiotics merely regulate the intestinal microbiota is to grossly misconstrue the role that probiotics play in human health.  They interact through a significant number of mechanisms: they produce short-chain fatty acids (SCFA) [4,5], enhance epithelia barrier integrity [6], modulate the immune system [7], influence hormone levels [8], produce enzymes [9], modulate gene expression [10] and studies have shown that probiotics can stimulate the enteric nervous system and affect gut transit time [11], and reduce visceral pain [12). Furthermore, L. reuteri has been shown to interact with the gut-brain axis in rats through the modulation of afferent sensory nerves that influence gut motility [13].

Although the mechanisms by which probiotics work are often underestimated, the mechanisms by which the FODMAP diet works are often overestimated. Studies have, with some consistently, shown that a FODMAP diet can alter digestive symptoms in IBS patients [14-17], yet it has not consistently been shown to do much else.

The exaggerated confidence given to the FODMAP diet, that it has the ability to favorably alter the intestinal microbiota, starve out organisms, or alter the immune system by reducing histamines, for example, are unfounded in the literature.  The diet is being misrepresented across publications, by practitioners and over social media, and in chat rooms.

When a study says “FODMAP DIET” what are they actually testing?

If you search the term ‘low FODMAP’ in, the results returned will include a wide variety of dietary intervention methods, all under the umbrella term ‘low FODMAP.’ As with most investigative feeding studies, the methods are far from uniform across the studies.

Some studies use a true dietary intervention, comparing a low FODMAP diet (LFD) and a high FODMAP diet (HFD). Some provide the food, but most are instructing the subjects on the diet (ranging from 10 minutes of instruction to 3 sessions with a dietitian). The diet is then self-followed and adherence is self-reported. Generally, a HFD is equivalent to 50 grams of FODMAP a day, and a LFD is equivalent to 1.2-9 grams of FODMAP a day (the majority of studies use a 7-9 gram per day range).

Some studies place participants on 14-16 grams of fructooligosaccharides (FOS) or galactooligosaccharides (GOS) for the HFD arm. Others compare a LFD diet to FOS alone. In some FODMAP studies, dextrin is used as the control, where a LFD + 16 grams per day of dextrin is compared to a LFD + 16 grams per day FOS. [18]

When we look closely at the studies on FODMAP, and their proposed effects on the microbiota and the immune system, the findings are inconsistent at best. What is agreed upon is that LFD helps to alter symptoms of bloating, diarrhea and quality of life, but even these studies have issues with quality, “All trials had high risk of bias (only one double‐blinded), intervention periods ranged from 2 days to 6 weeks with one including a 6 month follow‐up. …control diets were heterogeneous with limited established efficacy.” [19]

Some studies are also mislabeling the benefits of a LFD. In the article, “Is A Low FODMAP Diet Dangerous?,” the author states, “Shepherd et al. [20] at 14-month follow-up, found 77% of patients adherent to the (LFD) with 76% reporting significant improvement in abdominal symptoms” and yet, the Shepard et al. study referenced only altered fructose, which should not be misconstrued as a low FODMAP dietary intervention. [21]

What are we as practitioners trying to acheive by using an LFD?

You Want to Starve Out the Organisms?

Methane levels do not increase, nor decrease in response to a LFD nor HFD intervention, respectively, in ALL studies where this is measured. [22, 23, 29-31] There are three studies that show a change in hydrogen. Before I discuss these studies, let’s look at the Lactulose Breath Test (LBT) and how this test was validated for use.

The LBT is a diagnostic tool to detect levels of excess hydrogen and methane that is produced when the consumed test substrate, lactulose, passes by higher than normal levels of organisms in the small intestine (bacteria and archaea are able to digest and ferment this sugar, but we cannot). The excess gas produced exchanges across the intestinal tract, into the blood and then circulates and moves out through our lungs – where it is measured in breath samples.

This test is a validated laboratory test when, and only when, the subject has properly prepped for this test. This includes a 12 hour food prep, that occurs 24 hours prior to the test, of only fish, eggs, chicken, white rice and white bread (the latter two are allowed because they digest rapidly in the upper section of the small intestine). Then the subject fasts for 12 hours, and then waits two hours after getting out of bed in the morning (because morning breathing is more shallow) to take a baseline measure. The baseline measure is a control marker for the lab, to show that the test prep was done properly.

Then a standard dose of lactulose is consumed and depending on the lab, the subject is instructed to collect breath samples in 15 to 30 minute increments, for 90-180 minutes.

The proper 12 hour food prep reduces fermentation potential of the organisms that reside in the large intestine, whereby, we are able to get a clearer measure of gases in the small intestine as the lactulose substrate moves past the organisms.

If prepping incorrectly, this is simply a measure of the fermentation of food, fibers, and waste that is in the colon.

The LBT has also not been validated for use while the subject is eating during the period of time when collecting breath samples. This is no more validated than collecting a blood lipid panel while doing a non-fasting high fat diet. We all understand that the blood lipid panel will be affected by food that was recently ingested.

The LBT was validated to look at hydrogen and methane in the small intestine, which will occur within the first 90 minutes of the test. If a study collects breath samples while eating over a 10-14 hour period and then compares data points, what exactly are they measuring?

The first study – A Low FODMAP Diet Is Associated With Changes In The Microbiota And Reduction In Breath Hydrogen But Not Colonic Volume In Healthy Subjects: healthy subjects ate their habitual diet for 7 days, then provided a stool sample and swallowed transit markers. They were provided a 24 hour standard food package that was not LFD, and then completed a LBT the following morning. They followed a LFD for one week and then were randomized into two groups – the LFD control group was supplemented with maltodextrin. The HFD group was supplemented with oligofructose (prebiotic oligosaccharide, fructans). On the final day of the diet intervention they were provided a standard food pack that was LFD (not the correct LBT diet prep), followed by a LBT the following day. [32]

Concerns with this study:

  • The subject pool is healthy subjects – not IBS, nor SIBO.
  • Proper food prep and fasting were not performed for the LBT.
  • This is not a LFD vs. HFD food intervention. This is an LFD + dextrin vs. LFD + fructans intervention on healthy individuals.
  • The differences seen with hydrogen likely represent the differences in colonic fermentation of the standard food packages offered the day before the LBT.

The second study –  Randomised Clinical Trial: Gut Microbiome Biomarkers are Associated with Clinical Response to a LFD in Children with Irritable Bowel Syndrome: 33 children with IBS were monitored for 7 days on their habitual diet, they then were randomized into a 48-hour LFD or typical American childhood diet (TACD), followed by a 5 day washout, then crossed over to the other diet intervention for 48 hours. LBT was administered on day two of each intervention diet. Samples were collected for ≥ 8 hours, up to 15 hours, while they ate. [23]

Concerns with this study:

  • Proper food prep and fasting was not performed for the LBT.
  • They ate during the LBT.
  • LBT data was collected and analyzed over a 15 hour timespan.

This study did draw some interesting conclusions: “gas production did not correlate with pain, but may be a potential fermentation marker rather than a direct inducer of symptoms. Change in symptoms is more likely due to reduction in distention, reducing visceral hypersensitivity, than it is to sweeping uniform changes in the microbiota or immune system.”

The third study – one of the most cited studies within the SIBO world – Manipulation Of Dietary Short Chain Carbohydrates Alters The Pattern Of Gas Production And Genesis Of Symptoms In Irritable Bowel Syndrome: 15 healthy subjects and 15 IBS subjects were randomized into two groups. They ate either a LFD (9 grams per day) or HFD (50 grams per day) for two days, followed by a 7 day wash out period, and then crossed over to the other 2 day diet intervention.

Food was provided. From breakfast through lunch the LFD group was offered rice flakes, lactose free milk, tea, rice bread, margarine, orange juice, tea with lactose free milk, an orange, rice pasta with red sauce and lemonade with sugar. [15] Are we to use this menu, which is high in ‘white’ processed food and sugar, as a model to apply the LFD clinically?

Concerns with this study:

  • Proper food prep and fasting were not performed for the LBT
  • LBT data was collected and analyzed over a 14-hour timespan.
  • They ate during the LBT – we cannot then deduce from this data that a LFD or a HFD increases or decreases hydrogen.
  • They did not control for the timing of the meals that were consumed across the day. They provided the food and allowed subjects to choose when they would consume these foods across the day. Differences in hydrogen production could be due to timing with meals consumed, or, differences in transit time between the groups.

Though both groups had higher hydrogen levels in response to the HFD, the IBS group had higher levels than the healthy controls. There could be two reasons for this:

The first, this was due to what they were fed (stay with me here – I know that they were measuring diet). The HFD group was given soda with high fructose corn syrup.  With IBS, it has been shown that fructose malabsorption alone leads to osmotic diarrhea as well as gas and bloating due to excess fermentation in the colon, [20, 24-27] and not from FODMAPs in general.

Second, the increase in hydrogen could have also been a result of the sorbitol, in the two pieces of chewing gum that they were allowed, in combination with fructose from the HFCS soda. This combination has been shown to exacerbate symptoms by swiftly delivering malabsorbed carbohydrates to the colon, as seen in the study, Fructose-sorbitol ingestion provokes gastrointestinal symptoms in patients with eating disorders. [28]

There was a fourth study that reported a small difference in hydrogen production in response to a LFD, Fodmaps Alter Symptoms and the Metabolome of Patients with IBS: A Randomised Controlled Trial Mcintosh There was no statistical significance found when comparing baseline data to post diet intervention data. The authors then threw out the baseline data and had to adjust the post diet intervention data to find a statistical significance within groups of patients with IBS. Yet, they didn’t properly food prep their subjects for the LBT and they collected and analyzed LBT data over a 5 hour period. [22]

You Want To Change The Microbiome?

Studies that have investigated microbiota key traits in IBS are able to identify distinct profiles in the intestinal microbiota and organic acids [33], yet the idea that a LFD will directly treat this, is yet to be seen. To date, the LFD has been shown to reduce symptoms, but it has not been shown to directly treat the underlying mechanisms that are at the root of IBS and SIBO.

Strict FODMAP reduction shows unfavorable changes to the microbiota, with little known impact to long term health. A LFD reduces Bifidobacterium [34-36], it reduces beneficial SCFA [37], which could impair the bowel barrier function by leading to the apoptosis of epithelial cells [38,39]  and increase in proteolytic fermentation (fermentation of unfavorable BCFA versus SCFA). [40]

We can all agree that altering diet will alter the microbiome in some way. But the idea that we can use a LFD to cherry pick and reduce the specific species that are causing IBS or SIBO is unfounded. Additionally, another study found that the LFD made the microbiota more dysbiotic [18], in a group that has already been shown to have a dysbiotic microbiota. [41] “If dysbiosis is causal in IBS, although there is no direct evidence to support this, then the effect of a strict low-FODMAP diet might be counterproductive.” [42]

 Fodmaps Alter Symptoms and the Metabolome of Patients with IBS: A Randomised Controlled Trial Mcintosh LFD and the microbiome. There was no statistical significance found when comparing baseline data to post diet intervention data. The study states, “… No difference in alpha and beta diversity when comparing baseline samples and post treatment samples.” Yet, the study goes on to compare post intervention data only, making sweeping claims with regard to changes seen with the microbiome, in response to LFD vs. HFD diet. [22]

Two review articles summarized their investigation into IBS and the microbiota:

“… the investigation of the intestinal microbiota in IBS is difficult due to the heterogeneity of this condition, and the effects of an altered intestinal microbiota may not be consistent across all subtypes of IBS (D-IBS, C-IBS and M-IBS).” [43]

Based on the systematic review, “low FODMAPs appear to reduce gastrointestinal symptoms for a least a subset of patients with IBS. However, due to the heterogeneity of reviewed studies, the influence on patients’ gut microbiome composition and/or microbiota metabolites requires additional studies.” [44]

Do You Want to Alter the Immune System?

There is one study that has looked at HFD, lipopolysaccharides (LPS) and visceral hypersensitivity, mainly in rats, but also in 6 IBS-D patients. In 6 of the rats, it was found that fecal LPS was higher in the HFD vs. control diet (8.6 vs 5.1 EU/ mg).

The study claims that a HFD …”induces mucosal inflammation and impaired gut permeability,” yet, as we extrapolate this to humans, this is a stretch.  Rat chow, made to mimic a HFD,  with lactose, FOS and fructose added, may cause mucosal inflammation and impaired gut permeability in rats placed under one hour of constant stress per day (as they did in this study), but it will never correctly mimic a whole foods diet with altered FODMAP content. The authors do caution “It should be noted that rodent and human microbiota may differ significantly. Hence, caution should be exercised in extrapolating our data to explain human disease.” [45]

What is more of interest are the 6 IBS-D patients – it appears that the researchers preferentially chose their 6 subjects from a group of qualified participants, ‘Human fecal samples were collected from 6 patients showing significant reductions in abdominal symptoms before and following the 4-week LFM diet (LFD).’

Fecal samples were taken from the 6 human subjects, both pre and post-intervention and administered intracolonically into naïve rats. Pre- LFD intervention fecal samples increased visceral hypersensitivity in the rats. Post-diet intervention fecal sample did not increase visceral hypersensitivity.

From these results, should we infer that a person with IBS-D should be placed on a LFD long term? Isn’t it a more plausible conclusion from this 6 person hand selected group, that people with IBS-D and an elevated fecal LPS may benefit from following a 4 week elimination phase LFD and practitioners might consider a LFD as adjunct support, combining this with other clinical interventions that are known to help heal up leaky gut?

Additional studies have shown mixed results

In a mouse study, LFD did not exacerbate nor mitigate inflammation; noting that microbiota profile changes were largely driven by inflammation rather than diet and the LFD caused a shift toward proteolytic fermentation following inflammation. [46]

In a human study, they compared LFD + dextrin vs. LFD + FOS. The LFD showed improvements of symptoms, and a reduction in IL-6 and IL-8, but also a decrease in SCFA and an increase in colonic pH – TNF-alpha were unchanged. [18]

Another human study, Effect of diet and individual dietary guidance on gastrointestinal endocrine cells in patients with irritable bowel syndrome (Review)looked at changes in duodenal enteroendocrine cells in patients with irritable bowel syndrome following a LFD.  This review of the original study, by the same author, showed that 3-4 consecutive months on a self-followed LFD, increased serotonin production and the density of somatostatin cells, and quality of life; diarrhea and pain reduced, but constipation did not improve. [47] 46 IBS subjects started this study and only 14 subjects completed it (30% retention rate). This study was characterized by a high dropout rate, which is consistent with previous studies involving IBS patients. [8, 47-50]

In addition to the LFD, the subjects were also instructed to remove corn, legumes, wheat and artificial sweeteners from their diet. They included lactose free dairy products, alcohol and peeled apples and pears (the latter two are high in polyols and traditionally pulled with a LFD).

Is the increase in somatostatin cell density a result of a LFD, and/ or removing gluten, legumes, corn, and artificial sweeteners from the diet? Or, a combination of these AND a shift to whole foods eating; as removing gluten, corn, legumes and artificial sweeteners from a diet would force a shift from packaged foods to whole foods. [47]

Another question to ask – would these results reversed when the LFD is expanded, or when corn and wheat are reintroduced?

In conclusion

Before we continue to perpetuate this wave of fanfare for the LFD, we must first accept that the studies to date have offered mixed results, with the vast majority proving unfavorable. At this time, the LFD has consistently been shown to alter symptoms in some people with IBS.

We need further investigation into the long term effects on the microbiome and immune system. We need studies to implement the LBT in a validated way, so they may correctly interpret the impact of the LFD. “Inconsistencies between studies may be related to differences in habitual diets or differences in sample collection and analysis methodologies. The impact of these changes on gut function and symptoms remains to be elucidated.” [58] The impact on the intestinal microbiota specifically, has to be further investigated, before anyone can ‘safely’ implement a LFD long term.

In, The Pervasive Misunderstanding Of What The Fodmap Diet Does And Does Not Do – Part Two, I will discuss the misconceptions around LFD and histamine levels and how this is being incorrectly interpreted across current publications, LFD induced changes in nutrient status, the drawbacks to implementing a sweeping low FODMAP diet protocol clinically, and how to correctly implement the LFD into your clinical practice.

Angela Pifer, MSN, LN, CLN, FMN known as ‘SIBO Guru,’ has been in private practice for the past 15 years, blending functional medicine and integrative functional nutrition into evidence based work at her clinic in Seattle, Washington. She is an academic research practitioner, contributing to the field of functional gut disorders and  SIBO and through education and online tools, – a FODMAP recipe site and education that helps people expand their diet, and products, – the first commercially available low FODMAP bone broth,  that help people navigate and heal from SIBO. She carries a Master’s degree in Nutritional Science from Bastyr University and is a State Licensed Certified Nutritionist; training in Functional Medicine through the Institute of Functional Medicine.
(1)Yang B, Wei J, Ju P, et al. Effects Of Regulating Intestinal Microbiota On Anxiety Symptoms: A Systematic Review. General Psychiatry 2019;32:e100056. doi:10.1136/gpsych-2019-100056
(2) Eswaran, S, et al. A Diet Low in Fermentable Oligo-, Di-, and Monosaccharides and Polyols Improves Quality of Life and Reduces Activity Impairment in Patients With Irritable Bowel Syndrome and Diarrhea. Clinical Gastroenterology and Hepatology 2017;15(12):1890-1899.e3. doi: 10.1016/j.cgh.2017.06.044.
(3) Schumann D, et al. Randomised Clinical Trial: Yoga Vs A Low-FODMAP Diet In Patients With Irritable Bowel Syndrome. Aliment Pharmacol Ther 2018;47:203–11. doi:10.1111/apt.14400
(4) Gao, C, et alGut Microbe-Mediated Suppression of Inflammation-Associated Colon Carcinogenesis by Luminal Histamine Production. The American Journal of Pathology 2017;187(10):2323–2336. doi: 10.1016/j.ajpath.2017.06.011
(5) Sanders, ME, et al. Shared mechanisms among probiotic taxa: implications for general probiotic claims. Current Opinion in Biotechnology2018; 49:207–216. DOI: 10.1016/j.copbio.2017.09.007.
(6) Rao, RK & Samak, G. Protection and Restitution of Gut Barrier by Probiotics: Nutritional and Clinical Implications. Current Nutrition and Food Science 2013;9(2):99–107.
(7) Yan, F & Polk, DB. Probiotics and immune health. Current Opinion in Gastroenterology 2011;27(6):496–501. doi: 10.1097/MOG.0b013e32834baa4d .
(8) Clarke, G, et al. Minireview: Gut Microbiota: The Neglected Endocrine Organ. Molecular Endocrinology 2014;28(8):1221–1238. doi: 10.1210/me.2014-1108
(9) de Vrese, M, et alProbiotics–compensation for lactase insufficiency. The American Journal of Clinical Nutrition2001;73(2 Suppl):421S–429S. doi: 10.1093/ajcn/73.2.421s
(10)  Plaza-Diaz, J, et al. Modulation of immunity and inflammatory gene expression in the gut, in inflammatory diseases of the gut and in the liver by probiotics. World Journal of Gastroenterology2014;20(42):15632–49. doi: 10.3748/wjg.v20.i42.15632.
(11) Barbara, G, et al. Interactions between commensal bacteria and gut sensorimotor function in health and disease. Am J Gastroenterol 2005;Nov;100(11):2560-8. doi: 10.1111/j.1572-0241.2005.00230.x
(12) Pusceddu, MM & Gareau, MG. Visceral pain: gut microbiota, a new hope? J Biomed Sci 2018;25:73. doi: 10.1186/s12929-018-0476-7
(13) Kellow JE, et alPrinciples of applied neurogastroenterology: physiology/motility-sensation. Gut 1999;45(Suppl 2):ii17–ii24. doi: 10.1136/gut.45.2008.ii17.
(14) Halmos EP, et alA diet low in FODMAPs reduces symptoms of irritable bowel syndrome. Gastroenterology 2014;146:67–75.e5. doi: 10.1053/j.gastro.2013.09.046.
(15) Ong DK, et al. Manipulation of dietary short chain carbohydrates alters the pattern of gas production and genesis of symptoms in irritable bowel syndrome. J Gastroenterol Hepatol 2010;25:1366–73. doi 10.1111/j.1440-1746.2010.06370.x.
(16) Shepherd SJ, et alDietary triggers of abdominal symptoms in patients with irritable bowel syndrome: randomized placebo-controlled evidence. Clin Gastroenterol Hepatol 2008;6:765–71. doi: 10.1016/j.cgh.2008.02.058.
(17) Böhn L, et al. Diet Low in FODMAPs Reduces Symptoms of Irritable Bowel Syndrome as Well as Traditional Dietary Advice: A Randomized Controlled Trial. Gastroenterology 2015;149:1399–407.e2. doi: 10.1053/j.gastro.2015.07.054.
(18)  Hustoft, TN, et al. Effects of varying dietary content of fermentable short-chain carbohydrates on symptoms, fecal microenvironment, and cytokine profiles in patients with irritable bowel syndrome. Neurogastroentero and Motil. 2017  Apr;29(4). doi: 10.1111/nmo.12969.
(19) Krogsgaard LR, et alSystematic review: quality of trials on the symptomatic effects of the LFD for irritable bowel syndrome. Aliment Pharmacol Ther 2017;45:1506‐1513. doi: 10.1111/apt.14065.
(20) Shepherd SJ, et alFructose malabsorption and symptoms of irritable bowel syndrome: guidelines for effective dietary management. J Am Diet Assoc 2006;106:1631–1639. doi: 10.1016/j.jada.2006.07.010.
(21) Bellini, M et al. Is a low FODMAP diet dangerous?  Tech Coloproctol 2018;Aug;22(8):569-571. doi: 10.1007/s10151-018-1835-9.
(22) McIntosh, K, et alFODMAPs alter symptoms and the metabolome of patients with IBS: a randomised controlled trial. Gut 2016;66(7):1241–1251. doi:10.1136/gutjnl-2015-311339.
(23) Chumpitazi, BP, et al. Randomised clinical trial: gut microbiome biomarkers are associated with clinical response to a low FODMAP diet in children with the irritable bowel syndrome. Alimentary Pharmacology & Therapeutics 2015;42(4):418–427. doi:10.1111/apt.13286.
(24) DiNicolantonio JJ, et al. Is Fructose Malabsorption a Cause of Irritable Bowel Syndrome? Med Hypotheses 2015;Sep;85(3):295–297.doi: 10.1016/j.mehy.2015.05.019.
(25) Nelis GF, et al. Role of fructose-sorbitol malabsorption in the irritable bowel syndrome. Gastroenterology 1990;99:1016–1020. doi: 10.1016/0016-5085(90)90621-7
(26) Fernandez-Banares F, et al. Sugar malabsorption in functional bowel disease: clinical implications. Am J Gastroenterol 1993;88:2044–2050.
(27) Symons P, et al. Symptom provocation in irritable bowel syndrome. Effects of differing doses of fructose-sorbitol. Scand J Gastroenterol 1992;27:940–944.
(28) Friesen N, et al. Fructose-sorbitol ingestion provokes gastrointestinal symptoms in patients with eating disorders.  World J Gastroenterol 2009;Nov 14;15(42):5295–5299. doi: 10.3748/wjg.15.5295.
(29)Tuck, CJ, et al. Increasing Symptoms in Irritable Bowel Symptoms With Ingestion of Galacto-Oligosaccharides Are Mitigated by α-Galactosidase Treatment. The American Journal of Gastroenterology 2017;113(1):124–134.doi:10.1038/ajg.2017.245.
(30) Chumpitazi, BP, et al. Gut microbiota influences low fermentable substrate diet efficacy in children with irritable bowel syndrome. Gut Microbes 2014;5(2):165–175. doi:10.4161/gmic.27923.
(31) De Roest, RH, et al. The low FODMAP diet improves gastrointestinal symptoms in patients with irritable bowel syndrome: a prospective study. International Journal of Clinical Practice 2013;67(9):895–903. doi:10.1111/ijcp.12128.
(32) Sloan, TJ, et al. A low FODMAP diet is associated with changes in the microbiota and reduction in breath hydrogen but not colonic volume in healthy subjects. PLOS ONE 2018;13(7):e0201410. doi:10.1371/journal.pone.0201410.
(33) Tana, C, et al.  Altered profiles of intestinal microbiota and organic acids may be the origin of symptoms in irritable bowel syndrome. Neurogastroenterology & Motility 2009;May;22(5):512-9,e114-5. doi: 10.1111/j.1365-2982.2009.01427.x.
(34) Staudacher HM, et al. Fermentable Carbohydrate Restriction Reduces Luminal Bifidobacteria and Gastrointestinal Symptoms in Patients with Irritable Bowel Syndrome. Journal of Nutrition 2012;142(8):1510–8. doi: 10.3945/jn.112.159285.
(35) Halmos EP, et al. Diets that differ in their FODMAP content alter the colonic luminal microenvironment. Gut 2015;64(1):93–100. doi: 10.1136/gutjnl-2014-307264.
(36) Staudacher HM, et al. A Diet Low in FODMAPs Reduces Symptoms in Patients With Irritable Bowel Syndrome and A Probiotic Restores Bifidobacterium Species: A Randomized Controlled Trial. Gastroenterology 2017;153(4):936–47. doi:10.1053/j.gastro.2017.06.010.
(37) Hynonen U, et al. Isolation and whole genome sequencing of a Ruminococcus-like bacterium, associated with irritable bowel syndrome. Anaerobe 2016;39:60–7. doi: 10.1016/j.anaerobe.2016.03.001.
(38) Gibson P, et al. Personal view: Food for thought— Western lifestyle and susceptibility to Crohn’s disease. The FODMAP hypothesis. Aliment Pharmacol Ther 2005;21;1399– 1409. doi: 10.1111/j.1365-2036.2005.02506.x
(39) Durchschein F, et al. Diet therapy for inflammatory bowel diseases: The established and the new. World J Gastroenterol 2016;22:2179–2194. doi: 10.3748/wjg.v22.i7.2179.
(40) Valeur J, et al.  Fecal Fermentation in Irritable Bowel Syndrome: Influence of Dietary Restriction of Fermentable Oligosaccharides, Disaccharides, Monosaccharides and Polyols.  Digestion 2016;94(1):50-6. doi: 10.1159/000448280.
(41) Rajilic-Stojanovic M, et al. Intestinal microbiota and diet in IBS: causes, consequences, or epiphenomena? Am J Gastroenterol 2015;110(2):278–87. doi:10.1038/ajg.2014.427.
(42) Hill P, et al. Controversies and Recent Developments of the Low-FODMAP Diet. Gastroenterol Hepatol (N Y) 2017;Jan;13(1):36-45.
(43) Ian M Carrollet al. Luminal and mucosal-associated intestinal microbiota in patients with diarrhea-predominant irritable bowel syndrome. Gut Pathog 2010;2:19. doi: 10.1186/1757-4749-2-19
(44) Su H, et al. Effects of Low-FODMAPS Diet on Irritable Bowel Syndrome Symptoms and Gut Microbiome. Gastroenterol Nurs 2019;Mar/Apr;42(2):150-158. doi: 10.1097/SGA.0000000000000428.
(45) Zhou SY, et al. FODMAP diet modulates visceral nociception by lipopolysaccharide-mediated intestinal inflammation and barrier dysfunction. J Clin Invest 2018;Jan 2;128(1):267–280. doi: 10.1172/JCI92390.
(46) Tuck CJet al. The impact of dietary fermentable carbohydrates on a postinflammatory model of irritable bowel syndrome. Neurogastroenterol Motil 2019;Jul 9:e13675. doi: 10.1111/nmo.13675.
(47) Mazzawi, T, et al. Effect of diet and individual dietary guidance on gastrointestinal endocrine cells in patients with irritable bowel syndrome (Review). International Journal of Molecular Medicine (2017);40(4):943–952.doi:10.3892/ijmm.2017.3096.
(48) Everhart JE, et al. Irritable bowel syndrome in office-based practice in the United States. Gastroenterology 1991;100:998–1005. doi: 10.1016/0016-5085(91)90275-P.
(49) Spiegel BMR. The burden of IBS: looking at metrics. Curr Gastroenterol Rep 2009;11:265–269. doi: 10.1007/s11894-009-0039-x.
(50) Peery AF, et al. The burden of gastrointestinal diseases. Gastroenterology 2012;Nov;143(5): 1179–1187.e3. doi: 10.1053/j.gastro.2012.08.002
(58) Wang XJ, et al. Review article: biological mechanisms for symptom causation by individual FODMAP subgroups – the case for a more personalised approach to dietary restriction. Alimentary Pharmacology & Therapeutics 2019. doi:10.1111/apt.15419.

Enjoying this content? Sign up for updates... It's FREE!

Leave A Comment