SUMMARY: Learn impact of FODMAPS, Stomach Microbiome, Rifaximin… FODMAPS Diet helps over 70% of IBS likely because long term diet changes the microbiome in the stomach & gut. FODMAPS isn’t a life long diet; you reintroduce & learn your individual dosing limits.
Many now realize the need, if not necessity, to transition to a whole foods diet.
Foods from restaurants or cafeterias, prepared foods (even at sites considered healthy such as Whole Foods), and the obvious boxed foods make it tough for consumers to avoid caloric dense non nutritive foods with industrial seed oils and added chemicals, pesticides, and GMOs. The diet — health connection is becoming apparent; many suffering chronic disease(s) are trying to change diet and lifestyle to improve health and wellness. Eating whole foods can be daunting but the safest bet is making it yourself and to do so in quantity so as to make this lifestyle change sustainable:
I am going to walk you through and example using a typical low fat diet, to show how easy it is to need to turn to the whole foods table to remedy digestive health issues. Low fat dieters inadvertently increase carbohydrate loading in order to eat low fat; in doing so, they do not increase carbohydrate loads by eating more vegetables and low fructose fruits, rather grains and fructose dominant fruits dominate most low-fat diets. Top that off with the quality issue inherent in low fat prepared or processed foods as they generally contain many questionable ingredients, chemicals, GMOs and pesticides. The below slide drives home the macronutrient skew so you can see what 30 grams of carbs really looks like, two ways:
Many are now literally feeling the effects of such macronutrient skew either due to gluten sensitivity (or it could be due to another grain protein; we now realize that immunologic reactivity in celiac disease may not be limited to wheat gluten, but can involve certain nongluten proteins, too, see Nongluten wheat proteins triggered immune response in celiac patients), fructose malabsorption, or some other food intolerance/sensitivity). The end result is that many suffer with Irritable Bowel Syndrome (IBS) which is second to missed work days only to the common cold.
More IBS facts:
- IBS affects 10-20% of the general population, with women 20-40 years old accounting for the majority of patients. (2008 Clinical approach to irritable bowel syndrome, Astegiano et. al. 2008)
- Irritable bowel syndrome affects approximately 10-15% of the European population and up to 70% of individuals with IBS may not be formally diagnosed. (Quigley et. al. 2006)
- Patients with IBS cost a average $1300 more per year than non-IBS patients (Costs of care for irritable bowel syndrome patients in a health maintenance organization. Levy et. al. 2001)
- IBS results in more than $10 billion in direct costs (eg, office visits, medications) and $20 billion in indirect costs (eg, through work absenteeism and reduced productivity) each year.
(IBS – Review and What’s New, Foxx-Orenstein A. 2006)
- Approximately 12% of all primary care doctor visits are IBS related, making IBS one of the top 10 reasons people go to the doctor. (Total Costs of IBS: Employer and Managed Care Perspective, Cash 2005)
- Roughly 30% of all visits to a gastroenterologist are IBS related, making it the number one reason people see a gastroenterologist. (Total Costs of IBS: Employer and Managed Care Perspective, Cash 2005)
- IBS is the leading cause of missed work days in the US (second only to the common cold). (Total Costs of IBS: Employer and Managed Care Perspective, Cash 2005)
- IBS patients are more likely than others to have their gall bladder removed unnecessarily and with no positive effect on their IBS symptoms. IBS have an increased risk of cholecystectomy that is not due to an increased risk of gallstones, but rather to abdominal pain, awareness of having gallstones, and inappropriate surgical indications. (Gallstones, cholecystectomy and irritable bowel syndrome (IBS) MICOL population-based study, Corazziari et. al. 2008)
- The physician must realize that a strong physician–patient relationship will be the foundation for effective treatment and realistic expectations. Many patients with IBS have bounced around the medical field for many years with varying diagnoses because of the lack of interest or profound frustration by the physician in treating IBS, possible stigma of this disease as being a psychiatric entity, or lack of clinical, physical, or laboratory diagnostic criteria… The physician should also emphasize the chronic nature of this syndrome because nearly 75% of patients continue to have a diagnosis of IBS 5 years later.13 –Irritable Bowel Syndrome: A Review and Update, 2012
- A lot more citations to top IBS articles can be found at: Food Allergy and Intolerance Foundation (Selected Research Articles on IBS, Food Allergies, and Related Issues.Top Articles).
Rifaximin antibiotic treatment for IBS, seriously?!?
IBS is a serious issue; if it isn’t controlled the conventional treatment will use the antibiotic Rifaximin. Gastroenterology and Endoscopy News January, 2015 issue just reported that a second dosing of Rifaximin can be used since 2/3 relapse using one course Rifaximin (1,074 of 2,579): see Rifaximin Redo Benefits Some With Diarrhea-Predominant IBS (Abstract 45 presented at the 2014 annual meeting of the American College of Gastroenterology.) Also see American Gastroenterological Association Institute Guideline on the Pharmacological Management of Irritable Bowel Syndrome, Sept. 2014 for more IBS guidelines (generally recommends a lot of medicines, some are posted in Comment below).
The Role of Diet as provided in, Irritable Bowel Syndrome: A Review and Update, 2012, is a valid alternative for IBS:
Patients with IBS commonly complain that specific dietary misadventures contribute to their symptoms of abdominal discomfort, bloating, or exaggerated gastric-colic reflex (urgent bowel movement after eating a meal). The truth is that no specific food is likely the culprit because true food allergies are rare. It is merely the act of eating that most likely initiates these postprandial symptoms. Patients may begin to associate ingestion of certain foods such as fatty foods, caffeine, alcoholic beverages, carbonated foods, or gas-producing foods as the etiology of their complaints.2 The physician does not want to restrict the patients’ diet excessively because of the risk of encountering nutritional deficiencies. However, it may be a good idea to instruct the patient to limit suspected foods and slowly reintroduce these items individually to see if similar symptoms reoccur… [recommend] maintaining a daily food diary.
Cash et al demonstrated that lactose intolerance, one of the most common genetic disorders worldwide, was equally prevalent among IBS patients and the general population.14 Nonetheless, it is prudent that the physician have a high index of suspicion when symptoms of bloating, abdominal distention, and flatulence occur. By giving the patient a short course of a lactose-free diet, one can make a presumptive diagnosis of lactose intolerance if symptoms resolve.
One should always query the patient about the intake of foods containing sorbitol (i.e., sugar-free or diabetic candy and gum). Symptoms may be related to impaired absorption of carbohydrates in some patients. Specifically, one can target the fermentable oligo-, di-, and monosaccharides and polyols (FODMAPs). This group includes fructans, galactans, lactose, fructose, sorbitol, xylitol, and mannitol.15 Studies are limited documenting improvement in patients who restrict their diets of these foods; nonetheless, this is a safe option to consider.
CONSIDER GLUTEN-FREE DIET EVEN IF CELIAC DISEASE IS EXCLUDED:
In a study perfomed by Biesiekierski et al, patients with IBS without celiac disease reached satisfactory symptom control with a gluten-free diet, indicating that gluten was indeed a trigger of gut symptoms.10 This was a double-blind, randomized, placebo controlled study that only included 34 patients, but there was statistically significant improvement in overall symptoms, abdominal pain, bloating, satisfaction with stool consistency, and fatigue. However, the underlying mechanism of this sensitivity was not identified. Therefore, a trial of a gluten-free diet may be considered even though celiac disease was excluded in the initial work-up.
MORE ON FODMAPS, there are studies showing success:
Why might FODMAPS dietary intervention be effective in over 70% of IBS patients?
FODMAPS works since 75.6%, 37.8% and 13.3% of [IBS] patients had fructose, lactose malabsorption or small intestinal bacterial overgrowth respectively. – The low FODMAP diet improves gastrointestinal symptoms in patients with irritable bowel syndrome: a prospective study and see Clinical Ramifications of Malabsorption of Fructose and Other Short-chain Carbohydrates.
Helpful slides: Long term FODMAPS diet change would change up the IBS microbiome and for over 70% of IBS patients, symptoms become manageable; over 75% of patients adhere to FODMAPS.
The post, OPTIMAL MICROBIOME DIET FROM AMERICAN GUT DATA noted that long term diet change can change and modify a resilient and stable microbiome. Getting back to the low fat diet, a long term low fat diet would have created a resilient stable microbiome thus FODMAPS long term could change up that microbiome. But note: FODMAPS is not a life long diet. You reintroduce foods to learn your individual dosing and that unique diet is your long term diet.
We also now appreciate the role of antibiotics in nuking the gut microbiome (sometimes certain microbiota species never return) and the next question is:
What impact on microbiome does Rifaximin have?
Why you want to give DIET a chance and avoid rifaximin; here are some studies showing it does impact microbiome:
- Rifaximin Modulates the Vaginal Microbiome and Metabolome in Women Affected by Bacterial Vaginosis (Our data demonstrated the efficacy of rifaximin in restoring a health-like condition in terms of both bacterial communities and metabolomic features. In particular, rifaximin treatment was significantly associated with an increase in the lactobacillus/BV-related bacteria ratio, as well as with an increase in lactic acid concentration and a decrease of a pool of metabolites typically produced by BV-related bacteria (acetic acid, succinate, short-chain fatty acids, and biogenic amines). Among the tested dosages of rifaximin (100 and 25 mg for 5 days and 100 mg for 2 days), 25 mg for 5 days was found to be the most effective.) Note: I see BV resolve when live fermented vegetables (sauerkraut) is consumed, only 1 forkful a day:
Rifaximin and Crohn’s, Ulcerative Colitis and travellers’ diarrhoea microbiome impact: This study investigated the impact of the administration of 1800 mg/day of rifaximin on the faecal microbiota of four patients affected by colonic active CD… Rifaximin did not affect the overall composition of the gut microbiota, whereas it caused an increase in concentration ofBifidobacterium, Atopobium and Faecalibacterium prausnitzii. A shift in microbial metabolism was observed, as shown by increases in short-chain fatty acids, propanol, decanol, nonanone and aromatic organic compounds, and decreases in ethanol, methanol and glutamate. No genotoxicity or cytotoxicity was attributed to rifaximin, and conversely rifaximin was shown to have a chemopreventive role by protecting against hydrogen peroxide-induced DNA damage.
These results are in agreement with those obtained in a previous clinical study performed by administering the same dose of rifaximin (1800 mg/day) to patients affected by ulcerative colitis.47 Culture-dependent analysis of faecal samples showed that the antibiotic did not alter the concentration of some major bacterial groups, while it induced an increase in bifidobacteria. A recent study on the use of rifaximin (800 mg/day) in the treatment of travellers’ diarrhoea further confirmed that the clinical effectiveness of the antibiotic is not associated with evident alterations of the colonic microbiota.48
Conclusions: We demonstrated that rifaximin, neither disrupts the overall biostructure of the human microbiota nor exerts any cytotoxic or genotoxic activities, but it does provoke changes in bacterial metabolism and bifidobacterial numbers that support a functional advantage to the host. While not altering the overall structure of the human colonic microbiota, [rifaximin] increased bifidobacteria and led to variation of metabolic profiles associated with potential beneficial effects on the host. – Rifaximin modulates the colonic microbiota of patients with Crohn’s disease: an in vitro approach using a continuous culture colonic model system. My thoughts: Rifaximin can always be considered as a later treatment option if diet (SCD) fails to induce remission for IBD. Long term side effects of Rifaximin would need to be assessed. While Rifaximin is dubbed non systemic or non-absorbable, I am aware of Entocort users that needed to stop use due to burn like rashes occurring on the face and eyelid swelling. Obviously, it was systemically absorbed, via leaky gut perhaps? Seems intestinal permeability needs to be healed and for that, diet removing food intolerances is needed.
- See also rifaximin impact on gut/brain axis in Modulation of the Metabiome by Rifaximin in Patients with Cirrhosis and Minimal Hepatic Encephalopathy (rifaximin is associated with improved cognitive performance and reduction in endotoxemia in patients with cirrhosis and MHE. This was associated with a modest change in the stool microbiota characterization with reduced Veillonellaceae and increased Eubacteriaceae. There was a significant change in the serum metabolome with a specific increase in serum fatty acids after rifaximin therapy. Correlation networks showed that key bacterial families, Porphyromonadaceae, Bacteroidaceaeand Enterobacteriaceae had differing associations with the metabolome and microbiome after rifaximin compared to baseline linkages..)
And… Surprise: The stomach holds a core microbiome. How does Rifaximin affect that?
Stomachs help to digest food; they get the process rolling, boiling and grinding by coating our food in slime, enzymes and acid. This is the textbook explanation and no one is saying it is wrong, but its likely incomplete.
The stomach has long thought to be a sterile organ due to its acid production. Well… not any longer. The stomach holds a core microbiome: The human gastric microbiota: Is it time to rethink the pathogenesis of stomach diseases? 2015, provides:
Five major phyla have been detected in the stomach: Firmicutes, Bacteroidites, Actinobacteria, Fusobacteria and Proteobacteria. At the genera level, the healthy human stomach is dominated by Prevotella, Streptococcus, Veillonella, Rothia and Haemophilus; however, the composition of the gastric microbiota is dynamic and affected by such factors as diet, drugs and diseases.
Lots of things impact the stomach microbiome:
The long-term use of proton pump inhibitors (PPIs)
and H2-antagonists, as well as atrophic gastritis, affects
the composition of the gastric microbiota; this is not
surprising, considering that gastric microbiota depends
on gastric acid secretion. Bacterial overgrowth occurs
when the gastric pH was >3.8.23 Oro-pharyngeal-like
bacteria and fecal-like bacteria are significantly more
abundant in patients on PPI therapy than in patients
on H2-antagonists and untreated control subjects.24
Treatment for 2 weeks with PPI reduces gastric acid
secretion by 75% and this was sufficient to permit bacterial
colonization of the stomach in healthy volunteers.23
Omeprazole (40 mg/day) for 3 months induced
gastric bacterial overgrowth in 10 of 30 patients, compared
with 1 of 10 control subjects; however, after only
14 days of PPI treatment (omeprazole 30 mg/day), the
total number of gastric bacteria had increased to a significant
Antibiotics: Using culture-dependent and culture-independent
approaches, Mason et al.26 demonstrated
that cefoperazone treatment in the human
causes long-term alteration of gastric microbiota, such
as a significant reduction in the number of Lactobacilli
and overgrowth of Enterococci.
Relationship between Helicobacter pylori and
gastric microbiota — A shift in abundance of Firmicutes
phylum and the Streptococcus and Prevotella genera
can be found in the H. pylori-infected stomach and in
gastric cancer. See the article for more specifics.
The Sieve Hypothesis: Clever Study Suggests an Alternate Explanation for the Function of the Human Stomach, explains that increasing age (and dementia disease) showed decreasing stomach ph and differing microbiomes compared to thirty to forty year olds:
…key function of the stomach is to kill bad bacteria with acid. The acid, they argue, serves as a sieve. It stops bad bacteria, particularly the most opportunistic of pathogens, but it does not stop all bacteria. It lets those beneficial bacteria that have adaptations for dealing with stomach acid–adaptations honed over many thousands of generations–on down the gastrointestinal road. In their model, if the stomach fails to kill bad bacteria, pathogens dominate the intestines. They do so in place of the beneficial microbes that help our bodies to digest food and produce nutrients. And when they do… death or at least the failure to thrive is nearly inevitable.
…the pH of the human stomach increases with age; the stomach becomes less acidic. This effect is most acute in individuals over seventy years of age. In these individuals Orla-Jensen predicted that the stomach’s effectiveness as a killer of bad microbes might be compromised. In turn, the intestines, recipients of everything that leaves the stomach, living or dead, might become dominated by pathogenic species such as the weedy and deadly Clostridium dificile or by oral species, that while beneficial in the mouth can become a pathogen in the gut.
Bariatric surgery has the consequence of increasing the pH in the stomachs of those who have the surgery, making their stomachs less acidic. If the sieve hypothesis is right these individuals ought to have gut bacteria that look more like those of seventy years old than those of thirty year olds. They do. Recently a study has found that good Bifidobacterium species become more rare after bariatric surgery while oral bacteria (in this case Prevotella) and E. coli, which can be a pathogen, become more common. These results seem to be what the sieve hypothesis would predict. –The Sieve Hypothesis: Clever Study Suggests an Alternate Explanation for the Function of the Human Stomach. Also interesting, see Diet critical to improving type 2 diabetes after bariatric surgery, “the reduction of patients’ caloric intake following bariatric surgery is what leads to the major improvements in diabetes, not the surgery itself” which we now know is more accurately said that it also is the actual diet that modulates the microbiome that likely results in disease risk reduction.
What are the next stomach microbiome steps?
Tying disease with stomach microbiome: The human gastric microbiota: Is it time to rethink the pathogenesis of stomach diseases? 2015 predicts:
Future studies concerning gastric microbiota should
include microbial and metabolomic profiles, correlated
with the natural history of specific diseases.
Subsequently, germ-free animals could be used to
understand the casual relationship between bacteria
and host disease. Once this step is reached, the possibility
of modulating the gastric microbiota with the aim
to change the natural course of diseases, or to prevent
them, could be addressed.
Here is the ordinary diagnostic treatment plan for IBS as summarized in, Irritable Bowel Syndrome: A Review and Update, 2012, if you are interested:
…the physician should carefully perform a detailed history and physical to exclude other diagnoses with symptoms similar to those of IBS. The American College of Gastroenterology Functional GI Disorders Task Force stated that the current data do not support extensive testing in IBS patients.8 IBS patients do not appear to have a higher prevalence of organic disease than the general population. If no alarming findings exist such as weight loss, hematochezia, iron deficiency, and symptoms that are typical of IBS, routine diagnostic testing is not recommended.
…testing for celiac disease does seem reasonable in nonconstipating IBS… Sanders et al demonstrated that a higher prevalence of celiac disease exists in IBS patients (4.67%) compared with the general population (< 1%).9 However, a recently published study found that 1.7% of IBS patients were positive for TTG, and this was not different from the study group.10
Colonoscopy is acceptable in patients with a family history of inflammatory bowel disease; colon cancer; alarm symptoms, such as hematochezia, nocturnal or progressive abdominal pain, weight loss, anemia, elevated inflammatory markers, or electrolyte disturbances; or in patients over 50. When a colonoscopy is performed in patients with diarrhea-predominant IBS, random biopsies should be performed to rule out microscopic colitis.
If symptoms are not typical or alarm features are present, testing should include complete blood cell count, comprehensive metabolic profile, an inflammatory marker such as erythrocyte sedimentation rate or C-reactive protein, and thyroid stimulating hormone level. If diarrhea is predominating, fecal leukocytes and stool for Clostridium difficile when appropriate (such as patients with antibiotic use within 3 months or recent chemotherapy) should be obtained. Travel and social history may make stool tests for Giardia andCryptosporidium antigens appropriate. Serology for celiac disease, preferably the tissue transglutaminase or TTG- IgA, should be performed as part of the work-up for all patients suspected of having IBS associated with diarrhea or mixed subtype.
Now that you are aware, try the FODMAPS diet for IBS; there’s a very good chance you’ll change up your stomach microbiome and your gut microbiome for the better if you do such long term.
Digestion: You and Yur Microbiome Eats (lists conditions resulting from poor digestion)
Last updated: March 23, 2016 at 4:26 am for SEO optimization.
In health through awareness,