SUMMARY: Bottom Line of this post: You want OFF the IBS diseasepan! WHY? Because — putting aside pain, bowel issues, and bloat — IBS can alter the brain size and function in the emotion and sensory processing areas when having it a long time along with early life stressors [Labus et al., 2017], it is associated with A LOT of diseases, and there are A LOT of surgeries performed inappropriately because of misdiagnosis or poor manangement of IBS! DISEASES that are associated with IBS — the listing is NOT comprehensive — includes: Type 2 Diabetes, metabolic syndrome, fibromyalgia, chronic fatigue syndrome, IBD, CFS/ME, autism, anxiety, depression, MS, and Parkinson’s. Inappropriate SURGERIES occurring due to IBS misdiagnosis includes — appendectomy, cholecystectomy, ovarian, and hysterectomy. See below for All of those links. There are lots of ways to get off the IBS diseasespan! Learn in this post that it is YOUR choice: IBS, Microbiome, Fodmaps, Probiotics, Mindfulness-based stress reduction, Cognitive behavioral therapy works… or targeted drugs! Or not drugs — because of the poor efficacy of that current US standard of care: =&2=&“The physician should also emphasize the chronic nature of this syndrome [IBS] because nearly 75% of patients continue to have a diagnosis of IBS 5 years later.¹³” [Occhipinti et al., 2012]. “Many different drugs have been suggested for IBS treatment, but their real benefits are very debatable.” [Bellini et al., 2014]. Don’t be surprised. In 2012, the FDA changed the endpoints of those drug studies to stop being only one endpoint because of how multi factorial IBS symptomolgy is, and the Bristol Stool Chart — defining what is a ‘normal BM’ (which you’ll learn in this post) — despite being around since 1997, is only now being validated, 2016! Contrast all this to the UK British Dietetic Association guidelines for IBS — low FODMAP diet is the second-line intervention [Catassi et al., 2017] [McKenzie et al, 2016] [UK evidence-based practice guidelines for dietetic management of IBS in adults 2012 PDF])=&2=&as it helps about seventy-six percent of IBS patients [Magge et al., 2012] [Bohn et al., 2015] [Staudacher et al., 2011] and yet, it has come under attack with the current US standard of care still NOT recognizing the FODMAP diet (see this post). A rebuttal to all the rift recently published in 2017, authored by Monash University ressearchers, the creators of the FODMAP diet. See [Hill et al., 2017] To piggyback the diet fix, studies continue to find that probiotics might be something to think about for some cases of IBS — see [Whiteley, 2016]. Wondering about IBS and what early life stressors might mean? That group had more history of early life trauma (general trauma (31 items), physical (9 items), emotional (7 items), and sexual abuse (15 items)) AND they had longer duration of IBS symptoms. [Labus et al., 2017] While we can’t change our early life stressors, there are lots of ways to tackle IBS using diet, probiotics, mindfulness-based stress reduction, cognitive behavioral therapy and targeted drugs — according to the Monash rebuttal [Labus et al., 2017]. Now you know! Protect brain size and function, avoid potentially needless surgery and improve your disease status by fixing IBS; LISTEN to your gut! Unbelievable… check out the global prevalence of IBS:

DON’T OVERLOOK THE COMMENT SECTION to this post, it adds STUDIES PUBLISHING AFTER I WROTE THIS POST!

IBS is not a condition to ignore.

Address it & Resolve it considering: Diet (Fodmaps or similar and probiotics), mindfulness, cognitive behavioral, and/or target drugs because…

Many diseases, including those crossing the blood-brain-barrier, are associated with the condition, and resolution of the IBS may help prevent or mitigate the disease,
There are a lot of inappropriate surgeries performed due to misdiagnosis (or poor management) of IBS, and
It alters the brain emotion and sensory processing areas for those having IBS long term with early life stressors.

Great animation: What is IBS [Monash University]

Most people don’t even realize their symptoms are IBS — and yet IBS affects up to 10 to 25% of the population, and that has a large margin of error since few get counted via physician visits and the inclusion criteria differs. [Canavan et all., 2014]. I always recommend to jounal!

Links to the IBS Disease & Surgery Statistics

Most are surprised to learn that many diseases have IBS associations. Just to put that into perspective, 30–50% of patients diagnosed with IBD [endoscopically in remission] also report IBS-type symptoms.^{3, 4, 5}. [Ballou et al., 2017].   Check out the list of diseases having known IBS associations — it is not a comprehensive listing: Type 2 Diabetes  “Given the higher prediabetes occurrence in IBS, IBS may indirectly indicate a higher risk of Type 2 Diabetes.” [Gulcan et al., 2009], metabolic syndrome “The findings suggest that the treatment of irritable bowel syndrome may be a potentially beneficial factor for the PREVENTION of metabolic syndrome.”  [Guo et al., 2014], fibromyalgia (49% have IBS), chronic fatigue syndrome (51%), temporomandibular joint disorder (64%), and chronic pelvic pain (50%) [Heitkemper et al., 2015], IBD [Halpin et al., 2012], CFS/ME [Whiteley, 2017], autism [Navarro et al., 2016], anxiety and depression [Fond et al., 2014] see pdf here, Multiple Sclerosis [Marrie et al., 2015], and Parkinson’s [Mishima et al., 2017].

IBS is complex and multifactorial. It is “a disruption of the so called “brain-gut axis” that determines changes in the digestive motility and secretion, visceral hypersensitivity, abnormalities of enteroendocrine and immune systems, genetic factors, infections, alterations of the intestinal microbiota and inflammation could play a role in IBS.” [Bellini et al., 2014].

IBS costs society in terms of medical and loss work absenteeism over $21 billion annually. [Canavan et al., 2014] As well, more women (60 to 65%) are affected then men [iffgd, 2016], and lots of inappropriate surgeries due to misdiagnosis occur for IBS suffers. Some examples include appendectomy, cholecystectomy — 2 to 3 x more likely, and ovarian and hysterectomy (twice as likely) occurs 45 to 55% more often in IBS then controls. [=&4=&] [iffgd 2016] [Corazziari et al., 2008].

AND What is a Normal BM?!?

Wondering if you have IBS? Well.. what does a normal BM look like? Use the Bristol Stool Chart (BSC) — see TWO versions on the above journal pic — a ‘NORMAL BM’ is rated 3 to 5! IT FIRST PUBLISHED 1997 [Bristol Stool Chart 1997 PDF], BUT WAS ONLY VALIDATED FOR USE IN THE US IN 2016 BECAUSE IN IBS DRUG CLINICAL TRIALS, “There is little published evidence of efficacy for the most commonly used treatments. Thus, there is an urgent need to conduct clinical trials on existing and novel therapies.” See [Blake et al, 2016]  [Saps et al, 2016].  If still confused on what is ‘normal’, CHECK OUT A MODIFIED BSC VERSION AT [Lasch et al, 2016]. Honest… I am not making this up… validating the BSC in the US became a scramble because the [FDA Guidance, 2012} changed the “endpoints for clinical IBS trials since prior studies looked at one endpoint which can’t adequately report patient perspective of the complex IBS symptomology”!

The IBS Microbiome Study including early life stressors

The study: [Labus et al., 2017] Differences in gut microbial composition correlate with regional brain volumes in irritable bowel syndrome.

Cohort: 29 IBS adult patients and 23 healthy controls. Yes, the small cohort is a limitation of the study but as the study concludes: “the correlations of abundance of certain microbial taxa with early adverse life events and with distinct brain structural changes previously reported in IBS suggest a possible role of gut microbes and their metabolites in the development and shaping of the gut-microbiota-brain axis early in life, confirming results from a previous study [10]... Identifying IBS subgroups based on gut microbiota, their related metabolomic profiles and corresponding brain signatures is likely to play an important role in optimizing therapies in IBS.”

Questionaires used for early life stressors:

For background, in mice, early maternal separation induced the brain differences with consequent symptoms similar to IBS [Palma et al., 2015]. Moving to humans, the microbiome/IBS study [Labus et al., 2017] used The Hospital Anxiety and Depression Scale [HADs] [22], the Patient Health Questionnaire-15 [PHQ] for mood  [23], and the Early Traumatic Inventory–Self Report (ETI-SR) [24] for histories of childhood traumatic and adverse life events that occurred before age 18 years old covering four domains: general trauma (31 items), physical (9 items), emotional (7 items), and sexual abuse (15 items) [24]. Details on the ETI-SR are in the reference section at [Bremner et al., 2011].

The Catastrophizing subscale from the Coping Strategies Questionnaire assessed levels of catastrophizing [25]. The degree to which subject viewed situations as stressful in the past month was measured by the Perceived Stress Scale [26].

Medication usage included any of the following: antispasmodic, laxatives, stool softener, fiber supplement, nonsteroidal anti-inflammatory drugs, aspirin, acetaminophen, thyroid medications, antihistamine, or proton pump inhibitors. [Note… PPIs have a disrupted microbiome — see this post. The significance is that drugs likely need further stratification when evaluating microbiome.]

Findings: The IBS microbiomes clustered into two subgroups with those having early childhood trauma clustering together. This trauma could be influencing how the microbes in our gut interact with our brains as we grow, demonstrating a two-way street between the development of our nervous system and the microscopic residents of our digestive system.

One subgroup of IBS was indistinguishable from the healthy control cohort.

The other IBS subgroup differed and had an altered gut microbiota. As well, an area of the brain associated with pulling together the body’s sensory information was slightly bigger in this group. The front part of the insular cortex – an area associated with keeping certain body functions in balance as well as dealing with emotions and cognitive functions was slightly smaller as was the ventral prefrontal regions. This cohort also had more history of early life trauma based on a psychological evaluation called the Early Traumatic Inventory–Self Report (ETI-SR) Inventory, and a longer duration of IBS symptoms. “A history of early life trauma has been shown to be associated with structural and functional brain changes and to alter gut microbial composition. It is possible that the signals the gut and its microbes get from the brain of an individual with a history of childhood trauma may lead to lifelong changes in the gut microbiome. These alterations in the gut microbiota may feed back into sensory brain regions, altering the sensitivity to gut stimuli, a hallmark of people with IBS.” — Gut microbes linked to brain structure in people with irritable bowel syndrome, May 2017 UCLA Newsroom article. It was postulated that “different kinds of bacteria in the gut could be producing chemicals that influence the brain’s development during childhood. Traumatic experiences early in life could affect the brain, which in turn influences the kinds of microbes that grow in the gut. These in turn could influence the brain’s development”.— Bacteria Could Be Responsible For Shifts in Brain Structure in People With IBS, ScienceAlert May 2017.

Future — IBS clinical therapeutics

Your Choice: IBS, Microbiome, Fodmaps, Probiotics, Mindfulness-based stress reduction, Cognitive behavioral therapy and/or targeted drugs?!?

Part 1: Diet (Fodmaps & Probiotics)

“Analysis of a person’s gut microbiota may become a routine screening test for people with IBS in clinical practice, and future, therapies such as certain diets [low FODMAPS perhaps [Occhipinti et al., 2012]] and probiotics may become personalized based on an individual’s gut microbial profile.” [Labus et al., 2017]

Diet (Fodmaps)

What are FODMAPs? FODMAPs are food substrates that are poorly absorbed and therefore fermentable by the gut microbiota. The acronym stands for Fermentable Oligo-, di-, Monosaccharides And Polyols. FODMAP substrates are ubiquitous prebiotics in the diet that are difficult to digest for everyone, they are additive, and when in excess for your unique physiology, can cause digestive symptoms. “There is an accumulating body of evidence, based on observational and comparative studies, and on randomized-controlled trials that supports the notion that FODMAPs trigger gastrointestinal symptoms in patients with functional bowel disorders.” [Shepherd et al., 2013].

The FODMAP diet is not intended to be long-term therapy. From Monash University (the creator of the Low FODMAP diet): “A low FODMAP diet will reduce the intake of foods high in fibre and natural prebiotics, which in turn may impact of the growth of certain bacteria in the gut. This is why we advise against following a strict low FODMAP diet unnecessarily. Typically consume low FODMAP 2-6 weeks, then re-introduce FODMAPs in a deliberate process to learn tolerance levels using a FODMAP knowledgeable professional.” Source: Monash University, Dietary Fibre and natural prebiotics for gut health: FAQs. The below chart lists some prebiotic FODMAPs that beneficially feed the microbiome.

A FODMAP re-introduction guideline can be found at: Metagenics, Patient Information: Low FODMAP Diet for Irritable Bowel Syndrome.

Source: Monash University, Dietary Fibre and natural prebiotics for gut health: FAQs,

The efficacy of the elimination phase of the low-FODMAP diet for overall gastrointestinal symptom relief in adult patients with IBS has been seen in randomized, controlled trials; a blinded, randomized, rechallenge study; and observational studies that have been reviewed in detail elsewhere³^,⁴ as well as in a meta-analysis.⁵ These studies have shown that 50% to 86% of patients have a clinically meaningful response to the low-FODMAP diet. In contrast, the success of maintenance (the reintroduction phase of the diet) has been studied less (in only a few observational studies).⁶^,⁷ Due to the difficulties of designing an appropriately blinded, randomized, longer-term, interventional study, the evidence base for maintenance will likely remain less solid. [Hill et al,, 2017],

Dr. Gibson, the creator of the FODMAP diet, estimates that overall ~10% of the population may be FODMAP-sensitive. The book, The Complete Low-FODMAP Diet: A Revolutionary Plan for Managing IBS and Other Digestive Disorders, by Drs. Sue Shepherd and Peter Gibson is a reference guide and road map for the low-FODMAP diet.

Figure out if it is Gluten or FODMAP Intolerance!  The FODMAP gold standard of food intolerance testing (ie, food exclusion to achieve symptom resolution followed by gradual food reintroduction and subsequent symptom induction to identify tolerance)³⁵ is important because often gluten is not the dietary culprit contrary to many thinking otherwise. “Randomized studies have shown that there is a lack of gluten specificity in the induction of symptoms in the vast majority of patients with self-reported NCGS.³²^–³⁴ Another trial of 36 patients experienced improvement in gastrointestinal symptoms when placed on a low-FODMAP diet during the run-in period, but none had repeatedly consistent exacerbation of symptoms specifically on ingestion of FODMAP-depleted gluten during the blinded rechallenge phases.³¹ One logical interpretation of these studies is that the FODMAP reduction associated with avoidance of wheat, rye, and barley—all high in FODMAPs—led to partial response, and more extensive FODMAP restriction further improved that response.”  See [Hill et al,, 2017] for reference links.

IBS, Food Intolerances, and SIBO. FODMAPS may work since 75.6%, 37.8% and 13.3% of [IBS] patients had fructose, lactose malabsorption or small intestinal bacterial overgrowth respectively. [de Roest et al 2013]  [Barrett et al., 2007].

Disease and FODMAPs — IBD. The FODMAP diet successfully manages over 86% of IBS/IBD patients, having partial (54%) or full (32%) efficacy. Satisfaction with dietary management was seen in 83 (70%) IBS patients and 24 (55%) IBD patients. Eighty-four percent of patients lived on a modified low FODMAP diet (LFD), where some foods rich in FODMAPs were reintroduced, and 16% followed the LFD by the book without deviations. WHEAT, DAIRY products, and ONIONS were the foods most often NOT reintroduced by patients. [Maagaard et al., 2016].

Disease and FODMAPs —Diabetes. The Joslin Diabetes Center, a teaching and research affiliate of Harvard Medical School, recommends trying FODMAP for diabetes! Have IBS [and Diabetes]? Try FODMAPs.

Genetic predisposition and IBS. There may be a subset of patients that are genetically predisposed to IBS due to mutations in the gene encoding the enzyme sucrase-isomaltase which is responsible for the digestion of small carbohydrates from sugars and starches called disaccharides. 15Phe is a common sucrase-isomaltase polymorphism. “A significant decrease in the enzymatic activity of sucrase-isomaltase would be compatible with poor carbohydrate digestion in the intestine, possibly leading to malabsorption and bowel symptoms,” Hassan Naim, PhD. [Henström et al,, 2016] and see this Healio article.

Fructose and children under 10 years age: “Children under the age of 10 years have a reduced capacity to absorb fructose. It would be important to assess whether young children with IBS are consuming a high-FODMAP diet with excessive amounts of fruit/fruit products, dairy/dairy products, and wheat/wheat products. Furthermore, it would also be important to assess whether normalizing—that is, limiting portions of fruit, dairy, and wheat to reduce dietary intake of FODMAPs—results in symptom resolution.”  [Hill et al., 2017]

Probiotics — They Work Well for IBS!

The study. [Zhang et al., 2016]   Meta analysis of 21 randomized controlled trials (RCTs) that compared many probiotics including different types of Lactobacillus acidophilus and Lactobacillus rhamnosus including VSL#3 with placebo.

Conclusion: “Probiotics are an effective pharmacological therapy in IBS patients. Single probiotics, a low dose, and a short treatment duration were more effective with respect to overall symptom response and quality of life.” Some probitoic(s) worked very well but we don’t know enough about which ones used under which circumstances because the authors did not analyze “the effects of individual probiotic species”.

Practically, Try many different whole food probiotics. You’ll find those in the refrigerated section, or try making your own and see how you feel — see my Pinterest Ferment Board for starters. Always start   S—L—O—W! Here is the link for how I make SCD Yogurt – the FODMAP lactose is eliminated in this recipe since the long ferment time renders the yogurt lactose-free. Regarding the inflammatory casein protein, it is said that the recipe changes the protein to more digestible, but different milks can also be trialed to decrease the inflammatory nature of casein. If you find you still cannot tolerate yogurt, try non-dairy ferments such as those in the below pic. Note too: You should try those non-dairy ferments anyway because all ferments contain differing probiotic bacteria and more is better when it comes to talking microbiome diversity.

Part 2: Mindfulness-based stress reduction, cognitive behavioral therapy and/or targeted drugs?!?

Intro: Health psychology and gastroenterology have become increasingly aligned over the last several decades because: “There is strong evidence that cognitive behavioral therapy; hypnotherapy; and mindfulness-based therapy directly target physiological processes by reducing arousal of the autonomic nervous system, decreasing the stress-response, and even reducing inflammation. This physiologic effect is largely due to the so-called brain-gut axis, which explains in part the common gastrointestinal consequences of stress and anxiety. Although the brain-gut axis is particularly important in the treatment of IBS [and ALL diseases having IBS associations], it is also relevant among patients with IBD, especially when considering the increased likelihood of an IBD flare in the context of chronic stress.^{84, 85}” [Ballou et al., 2017].

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