Category Archives: Blog: IBD

Healthy Pregnancy Diet. Melody Trial is now recruiting

Summary. If you are a pregnant mom (less than 27 weeks pregnant), or planning to become pregnant and wondering about a healthy pregnancy diet, please consider participating in the MELODY Trial, ClinicalTrials.gov Identifier: NCT03850600, WHICH IS NOW RECRUITING! I am super excited about this trial because it is recruiting pregnant aged women to participate in a study that will evaluate the efficacy of a diet intervention during the third trimester of pregnancy. The study’s goal is to determine if manipulation of the mothers microbiome, through diet, would benefit their baby. The diet aims to promote a healthier immune system during a critical time of immune system development.  I am helping to recruit for the trial which will have 396 participants, having and not having autoimmune Crohn’s disease. Details for the trial are below. Guys, if the MELODY Trial works for IBD, to improve the microbiome and baby’s immune system, will this strategy work for other diseases?!? Please, do your part and share this info with your friends, daughters, gynecologists, GI docs, doulas… Lets load this cohort quickly and move the needle to make the future better for our next generation! We’ve messed so many things up microbiome-wise, WE OWE OUR CHILDREN THIS!

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IBS, New Blood Test!

SUMMARY: There is a SIMPLE IBS new blood test in town that can diagnose the IBS sub-type that is due to a previous food-borne illness with 95% certainty, in 5 to 10 business days after blood draw. It is for those with IBS-D (diarrhea predominant) OR IBS-M (mixed type: diarrhea and constipation) symptoms. The test is called Ibs-smart (from Gemelli Biotech) and it costs $220 (insurance may cover it in part). IBS is an umbrella term, and up until now, diagnosis was by method of exclusion, when all other $$$$ and mostly very uncomfortable tests (like colonoscopy, upper endoscopy, CAT scan, and MRI) have ruled out other potential causes for symptoms. 15% of the population contracts food borne illnesses each year putting many at risk for developing this IBS sub-type! Further, this IBS sub-type is being considered to be AUTOIMMUNE so it is important to get it into remission. Otherwise, you open up Pandora’s box to developing other disease(s) and of undergoing inappropriate surgeries Ibs-smart™ is B-I-G news for IBS because IBS affects 10 to 15% of the population (according to credible reporting agencies). Not surprising, those stats are LOW for many reasons (mostly people suffer in silence and doctors don’t correctly diagnosis IBS). [Canavan et al 2014]. Heck, only about 50% of patients with IBS are provided with a definitive diagnosis after seeing a physician. [Halpert 2018]. The beauty of Ibs-smart™ is that if it is positive, you know you have IBS, that it is from a previous food poisoning, and you should think about this condition as autoimmune so get it into remission! Further, you know that IF you get food poisoning AGAIN, you are more susceptible to increasing those antibodies and making your IBS symptoms worse! Learn more about all of this below!

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Melody TRIAL- Can Maternal Diet Reduce Disease Transmission to the Newborn?

SUMMARY: I am beyond excited to begin 2019 with the announcement of a groundbreaking microbiome study that I’ve been asked to help spread the word on! The study, called the MELODY trial, peels back the layers of microbiome influence further than any study I’ve seen to date because it moves the needle for microbiome manipulation PAST the immediate host to hopefully influence and alter the health of the newborn! HOW? The MELODY Trial will recruit childbearing aged women to investigate if changing the maternal diet can reduce transmission of disease to the newborn! The Melody Trial will focus on Inflammatory Bowel Disease (IBD) because children born to mothers with IBD have increased risk of IBD. Participant recruitment is targeted to begin mid-January, 2019. Its website is coming soon, and I’ll post that info ASAP! However, to start this discussion and catch all up to speed, this post explains another study called the MECONIUM Study (see the link here) and its EIGHT publications are below! MECONIUM stands for Exploring MEChanisms Of disease trasmission IUtero through the Microbiome. I’m starting here because the MELODY trial is based on the preliminary findings of the MECONIUM Study! The primary investigating lab for both studies is Peter Lab, Icahn School of Medicine at Mount Sinai. The MECONIUM Study was a prospective study that explored the role IBD plays in the composition of the maternal and infant microbiome. The MECONIUM Study found that the dysbiotic microbiome seen in infants born to mothers with IBD can be improved when ENVIRONMENTAL factors known to have a negative effect on the microbiome are ABSENT in early life. In particular, the sub-optimal microbiome of babies born to IBD mothers were MITIGATED in early life when the baby was born vaginally, was not exposed to antibiotics, and was exclusively or partially breastfed.  Because of these findings, and since DIET is also considered an environmental factor that can change the  gut microbiome, the MELODY Trial investigates if IBD mothers consuming the UMass IBD-AID diet (a diet shown to change the gut microbiome to anti-inflammatory, aid in repair of the gut, and help restore balance to the immune system to help induce remission for IBD), also alters the  vaginal microbiome and reduces the risk of transmitting the dysbiotic disease-prone microbiome to the newborn.  Guys, if the MELODY Trial works for IBD, will this strategy work for other diseases?!? Please, do your part and share this info with your friends, daughters, gynecologists, GI docs, doulas… Lets load this cohort quickly and move the needle to make the future better for our next generation! We’ve messed so many things up microbiome-wise, WE OWE OUR CHILDREN THIS!

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IBS, Microbiome, Fodmaps, Probiotics

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., 2014see 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
  • 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.3234   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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Concise Summary of SCD Studies

SUMMARY:  Here is the Concise Summary of Specific Carbohydrate Diet, or SCD Studies with a focus on SCD for dietary treatment for Inflammatory Bowel Disease (IBD).  Actually though, SCD is used for many conditions, not just IBD.  This post focuses on the boatload of studies evaluating SCD for IBD because that is where most of the SCD research is happening.  Make sure you look at the comments below this post for even more links to studies that have published since I released this post.  You’ll even see that modified versions of SCD are also in study for IBD like PRODUCE, CDED, CD-TREAT, IBD-AID, Low FODMAP, Mediterranean! [Sabino et al 2019]. The findings support that once gut irritating foods are removed, the immune system changes because the gut microbiome changes. That should be true for whatever condition SCD is used for.  Take this Round-table of SCD studies to your doctor and ask for support especially if for IBD.  They should liaison with those already integrating the SCD into IBD dietary therapeutics.  SCD helps IBD with or without medications and can be used to induce remission for many with and without medications.  Always, the goal of treatment is IBD remission, not necessarily medication-free.  Half of the 417 patients surveyed [Suskind et al., 2016] use the SCD to induce remission; the other half use it adjunct to medications because of medication failure.  Think how many guts could be saved!  Dr. David Suskind (leading light GI at Seattle Children’s  Hospital integrating SCD into IBD clinical  dietary therapeutics) explains [Suskind Dietary Treatment  YouTube, 2016] that some use SCD alone if with mild to moderate symptoms at diagnosis.  Others use SCD along with medications and then once in remission, it may be possible to wean off medications.  Consider giving some of the SCD tenets (especially the emulsifier elimination) a try regardless of your disease, or for aggressive  preventative health.  Diet that removes gut irritants is that powerful because it changes up the microbiome where over 70% of immunity resides!  What do you have to lose????  

FYI:  Portions of the following are excerpts taken from a letter that I wrote for purpose of hospital affiliated clinical integration of SCD into IBD therapeutics!  IF you are similarly advocating, write me for insights!

Remission for IBD using the Specific Carbohydrate Diet (SCD)

SCD has been shown in small human case series to be effective for inducing and maintaining remission in

Furthermore, modified versions of SCD are now in study including: PRODUCE, CDED, CD-TREAT, IBD-AID, Low FODMAP, Mediterranean and more, see Figure 1 in  [Sabino et al 2019] for comparison of permitted and omitted components.  Also read the comments below this post for more!

The primary benefit of dietary therapies in IBD

The primary benefit of dietary therapies in IBD, as either primary or adjunctive therapy, has been the potential to decrease surgery (they keep their intestines), the exposure to immunosuppressive medications and their associated adverse effects, and seeing growth occur for these children.

SCD timing.  I can tell you from personal experience, acclimating children while still living with parents/primary care givers to SCD is incredibly easier for transition when moving into college then those only becoming aware of SCD while in college.  Dr. Suskind’s 2016 presentation specifically notes that they likely would not encourage use of the SCD for those newly diagnosed in the senior year of high school who are transitioning to living away from home at college.  My experience however… it can be done!

What SCD is Food-wise

For background, the SCD  was first described by Dr. Sidney Haas in 1924 as a means to treat celiac disease [Hass 1955].  It was popularized by biochemist Elaine Gottschall who added the science explaining how the diet works in the book (as well as the website), Breaking the Vicious Cycle.  Dr Gottschall studied and used SCD to cure her daughter of UC and avoided surgical colon removal.

What the SCD foods are in simpleton

SCD is an elimination diet

The SCD removes emulsifiers, maltodextrin and other processed food additives and preservatives, grains, grain derived flours and all true and pseudograins, milk (fermented lactose-free is permitted), some vegetables (potatoes, okra, corn), and sweeteners (except honey).

The SCD allows:
  • almost all fruits,
  • vegetables containing more amylose (a linear-chain polysaccharide) than amylopectin (a branch-chained polysaccharide),
  • nuts, nut-derived flours,
  • dry-curd cottage cheese,
  • meats, fish, poultry,
  • eggs,
  • Lactose-free cheeses. Lactose, a disaccharide not allowed in the SCD.
  • Lactose-free homemade yogurt using starter culture:  Lactobacillus bulgaricus, Lactobacillus acidophilus, Streptococcus thermophilus, and Lactobacillus rhamnosus — this was later added once it was discovered it had been included in probiotic capsules used for the yogurt from early days. SCD yogurt is fermented 24 to 30 hr to be free of lactose.
  • butters, and oils.

The typical starting dieter begins eating foods that are thought to be well tolerated, including cooked, peeled, and seeded fruits and vegetables, and over time other foods are added slowly to partially liberalize the diet.

Update April 22, 2017:  the Nutritional Adequacy of SCD is confirmed and explained by Dr. Suskind’s RD, Kimberly Braly in this April 9, 2016 presentation.

What the SCD foods are in techno verbage

The underlying theory of the SCD is that di- and poly-saccharide carbohydrates are poorly absorbed in the human intestinal tract resulting in malabsorption, bacterial and yeast overgrowth, and subsequent overproduction of mucus. These effects are hypothesized to result in small bowel injury thus perpetuating the cycle of carbohydrate malabsorption and intestinal injury.  This could cause compromised digestive enzymes, alterations in microbiome composition, intestinal gut inflammation, and consequent gut barrier dysfunction.

Another mechanism for IBD gut damage is the ubiquitous emulsifier additives in food.  In mice, they change the microbiome to pro-inflammatory which degrades the mucosal lining and induces IBD (as well as Metabolic Syndrome) [Gewirtz et al. 2015].

The SCD works around these gut irritants by eliminating processed foods (so no emulsifiers) and permitting carbohydrate foods consisting of monosaccharides only (so absorption is above the intestinal area of damage) and excludes disaccharides, most polysaccharides (such as linear or branch-chained multiple sugars or starches), and sucrose, maltose, isomaltose, lactose.

SCD mechanism of action and microbiome studies

The bacterial component of IBD.  It is unequivocal that IBD gut microbiome is skewed.  For those details, read the post where Dr. Rob Knight discusses the IBD microbiome skew, which also discusses W. A. Walters et al. 2014, Meta-analyses of human gut microbes associated with obesity and IBD.  The finding was that IBD has a consistent microbiome signature across studies and allows high classification accuracy of IBD from non-IBD subjects.

The fungal component of IBD.  Case Western researchers [Hoarau et al. 2016] are one of the first to look beyond the bacterial component of the microbiome and move to the fungal component.  Their study links two bacteria (Escherichia coli and Serratia marcescens) and one fungus (Candida tropicalis) as elevated and moving in lock step for Crohn’s.  In test tube they find  the three work together (with the E. coli cells fusing to the fungal cells and S. marcescens forming a bridge connecting the microbes) to produce a biofilm — a thin, slimy layer of microorganisms found in the body that adheres to, among other sites, a portion of the intestines — which can prompt inflammation that results in the symptoms of Crohn’s disease.

The literature explains that the mechanisms by which the SCD works may come from alteration of the gut microbiome or barrier function via differences in macronutrients or removal of certain dietary exposures such as emulsifiers and  maltodextrin [Martinez-Medina et al. 2014Chassaing et al. 2015; Gewirtz et al. 2015Nickerson et al. 2015].   The SCD eliminates emulsifiers.  For emulsifier induction of IBD in mice (and Metabolic Syndrome in mice having normal immune system) with consequent microbiome change, read the post, MICROBIOME, EMULSIFIERS, IBD & METABOLIC SYNDROME.

Suskind, et al, 2016 discusses that targeting two pathophysiological components of IBD, the microbiota and barrier function, as new primary or adjunctive therapies for IBD, holds great promise and his clinic is one of several on the forefront of integrating SCD into clinic therapeutics successfully.

The follow-up SCD human microbiome studies [Walters, et al. 2014Suskind, et al, 2016]; Suskind, et al, 2016] are providing further evidence of microbiome changes eating SCD that support the integration of SCD into IBD clinic therapeutics.  Lead SCD investigator Dr. Suskind explains in this Healthlink Special: Specific Carbohydrate Diet, that dietary therapy changes what the immune system reacts to.  Dietary therapy changes the microbiome in the gut. The published microbiome studies now show that removing gut irritating food changes the gut microbiome.

Walters, et al. 2014 found that:  

  • At baseline, before SCD implementation, overall microbial diversity was significantly decreased in IBD samples as compared to the healthy negative controls. IBD patients had more Bacteroides fragilis and a decreased abundance in Clostridium lactatifermentans, indicating a shift in the microbiota away from the composition of the microbial communities in the healthy controls.
  • SCD increased microbiome diversity whereas the low residual diet (LRD) decreased microbiome diversity.  
  • Interestingly, the SCD diet included an increased microbiota representation of F. prausnitzii, an anti-inflammatory commensal often called a peace-keeping microbe.  The post, NICE, EATING SCD INCREASED F. PRAUSNITZII… HUGH?!? explains the significance of F. prausnitzii in the microbiome.
  • Noteworthy:  Patient SCD diet COMPLIANCE was only about 80%.  Stanford child study Burgis et al. 2016, similarly found that non-compliance following varying lengths of strict SCD still maintained significantly reduced inflammatory IBD biomarkers and disease symptomology albeit those strict SCD had better results.   
  • Also noteworthy:  The SCD MICROBIOME DIVERSITY REMAINED despite a 30 day washout between diets when participants ate their pre-SCD diet.

UMass IBD-AID diet.  There is another diet being studied that is based on the SCD.  This diet is called the UMass IBD-AIDUniversity of Massachusetts Medical School, Center for Applied Nutrition. UMass IBD-AID is based on SCD with the addition of a few more microbiome supportive foods and is presently in  microbiome human clinical trial.  The Olendzki, et al. 2014 studies highlight five components by which diet modulates the IBD microbiome.   UMass showed in,  An anti-inflammatory diet as treatment for inflammatory bowel disease: a case series report, that aSCD modified dietary protocol can be used as an adjunctive or alternative therapy for the treatment of IBD.  Notably, 9 out of 11 patients were able to be managed without anti-TNF therapy, and 100% of the patients had their symptoms reduced.” 

SCD and Mediterranean-style diet to induce remission.  The Crohn’s & Colitis Foundation of America awarded $2.5 million from the Patient-Centered Outcomes Research Institute  to study the effectiveness of the SCD and Mediterranean-style diet to induce remission in patients with Crohn’s disease.  See the release here.  

Understand that while medication-free is the goal for many eating the SCD, it does not work for all. Some still need medications along with SCD for remission due to the failure of medication alone. 

In this regard, the SCD microbiome studies find that the efficacy of the medications are improved when combined with eating SCD.

  • For example, Walters, et al. 2014 finds the IBD microbiome on medications moves from high dsybiosis pre-SCD to healthy (more diverse and rich) with SCD.  Also notable, this study found that one month of eating SCD allowed persistence of the more healthful microbiome (increased diversity) for a full following month of eating pre-SCD diet foods during the washout period.   
  • Dr. Suskind’s presentation dittos that SCD increases efficacy of medications and can be heard at YouTube:  Nutrition Suskind Dietary Treatment Of IBD 2016 04 09.

Increasing medication efficacy is important because surgery risk is great if remission is not sustained. Medication efficacy for IBD remission:   “[The] current mainstays of IBD treatment are expensive anti-inflammatory and immunosuppressive drugs. Among those who can afford to be on treatment, approximately 40% are either unresponsive to any of the available drugs or cannot tolerate them. The chances that an IBD patient responds to medications and remains flare-up-free after 1 year on even the most potent medications, such as TNF inhibitors, is as low as 20–25%. Furthermore, medical therapy of IBD carries significant risks, among which are life-threatening infections, cancers (especially lymphoma) and neurological complications, such as demyelinating disease…  By comparison, diet therapy has the potential to be safe, lifelong and relatively cheap.”  – “To diet or not if you have inflammatory bowel disease”, 2014,  Expert Review of Gastroenterology & Hepatology, Informa Healthcare.

Regarding SCD and noncompliance

Regarding SCD and noncompliance, Stanford child study Burgis et al. 2016, found that non-compliance following varying lengths of strict SCD still maintained significantly reduced inflammatory IBD biomarkers and disease symptomology albeit those strict SCD had better results.  These researchers are currently completing a prospective pilot study of pediatric patients with Crohn’s Disease on the SCD investigating the impact on disease activity, inflammatory markers including fecal calprotectin, cytokine profiles and intestinal microbiota populations.

Walters, et al. 2014 found thatatient SCD COMPLIANCE was about 80%, and for this study’s cohort, SCD increased microbiome diversity whereas the low residual diet (LRD) decreased microbiome diversity.  Further,  SCD INCREASED MICROBIOME DIVERSITY REMAINED despite a 30 day washout between diets.

Individualization of dietary therapy for IBD.

Lee et al., 2016 discusses the likely need for individualization of dietary therapy for IBD.  Personally, I see this need not just at the start of SCD, but throughout the mucosal and microbiome normalization time frame probably partly due to FODMAP.   Knight-Sepulveda et al. 2015 noted the efficacy of the FODMAPs diet for IBD and that efficacy increases with increasing diet compliance.  Nanayakkara et al, 2016 discusses FODMAPs in depth and notes that IBS symptoms were found to improve for both Crohn’s and UC using the FODMAPs diet.

Once in remission using diet, non-SCD foods can be successfully re-introduced

Once in remission using diet, Dr. Suskind [Suskind Dietary Treatment  YouTube, 2016] explains that non-SCD foods can be successfully re-introduced if the patient so chooses, in a structured manner that ensures tolerance evaluating symptoms, serum inflammation, and fecal calprotectin levels.  Different people respond differently to foods added.  Inflammatory biomarker labs and fecal calprotectin levels prior to food re-introduction are compared to levels following four weeks of eating the food three times each week.  Obviously, re-introduction stops if symptoms become apparent.  Common foods that have successfully been re-introduced (one at a time) in Dr. Suskind’s clinic include:  Gluten-free oats, rice, cocoa powder/nibs, quinoa, potatoes, chick peas.  It is interesting that some of the foods Dr. Suskind trials for re-introduction are those which the UMass IBD-AID (a somewhat more microbiome supportive diet heavily based on SCD) permits.

Dr. Suskind Conference on How to Integrate SCD into Clinic Therapeutics

In 2016, Seattle Children’s Hospital presented for Continuing Medical Education, a program detailing how to integrate SCD into clinic.  Dr. Suskind’s insightful presentation can be heard at YouTube:  Nutrition Suskind Dietary Treatment Of IBD 2016 04 09.  Key points are (but listen yourself for your own pearls):

  • The SCD is combined with laboratory markers of inflammation to ascertain tolerance and response for IBD.  Mild to moderate IBD may use SCD for induction of remission while more severe would combine medications with SCD to induce remission.  Weaning of medications may then be possible.  But the focus is not medication-free, rather remission.  One test run for a measure of gut inflammation is fecal calprotectin.  Most all people that I cross paths with have never heard of the fecal calprotectin.  I am grateful awareness is increasing for fecal calprotectin but note Pittsburgh gastroenterologists seem to not yet follow this protocol unless the outside physician prescribes the labs.
  • Typically, the SCD intro diet is eaten as short as possible but up to 1 to 2 weeks max and consists of broth, SCD yogurt, applesauce, meat and eggs. The maintenance diet follows with adds of one food (honey, nuts, meats, fish, fruit, vegetables) every 1 to 2 days.
  • At 2 week followup, there is mild improvement of symptoms and some weight loss of 1 to 2%.  If however there remains a lot of symptoms then medications can be added.  At the 4 week followup, clinical remission is achieved and inflammatory markers normalize.  Discussion centers around what is working, what isn’t working, and problem solving with emphasis on eating diversity of diet.  Clinically, mild symptoms can persist for about 2 months. Clinical response but mild inflammatory marker elevation can often occur for up to 3 months.
  • At 12 weeks, things are going really well.  Emphasis is to stay strict SCD because of such great health, but discussion occurs on food re-introduction which is controversial in the general SCD community.  If at 3 to 6 months, the patient is asymptomatic and in remission, they will entertain food re-intro in a step wise fashion that follows inflammatory markers and fecal calprotection comparisons prior to and after food re-introduction.  The trial is 3 times a week eat the one new food for four weeks. Common foods reintroduced are: rice, gluten-free oats, cocoa powder/nibs, quinoa, potatoes, and chick peas.  Different people respond differently to new foods.  Some are able to add in many new foods, others none.
  • Regarding probiotics, most families do the SCD yogurt and ferment component.  The best though is the SCD diet which is actually a prebiotic meaning the SCD diet feeds and promotes the growth of beneficial microbiome flora within the gut.
  • In 2016, they had about 60 patients eating SCD with most doing quite well.  It seems that Crohn’s has better success than UC.  Dr. Suskind estimated that it will take about 5 years until SCD will be available in clinics across the US.  Integration of the science into clinic therapeutics is slow.  Geez… That is a lot of gut harm happening because the meds don’t stop the inflammatory gut microbiome.
  • A 504 Plan for disability is very helpful to permit greater leniency for snacks in classes, etc.  My college SCD/IBD find it very helpful.
Patient interest in SCD is strong and sustained

Dr. Suskind’s 2016 presentation notes that IBD patient interest in SCD is strong and sustained.  This is consistent to that also found in the 2015 James Lind Alliance Priority Setting Partnerships  literature.  

Patient interest is two fold [Suskind et al., 2016]:

  1. Half of a 417 patient survey use the SCD because of hesitation with medications used for IBD, and
  2. The other half use SCD because the failure of medications to induce remission necessitates the add-on of SCD trial for induction of remission.

Details for the 417 patient survey [Suskind et al., 2016]:  This survey was conducted online using known SCD Web sites and support groups in an attempt to characterize patient utilization of the SCD and perception of efficacy of the SCD.  Most of the 417 respondents use the SCD as a primary and adjunct therapy for IBD.  Most patients perceive clinical benefit to use of the SCD.

In Kakodkar et al. a 50 cohort, 2015, the majority of the SCD followers prefer SCD due to fear of long term consequences of medications (82%,) efficacy of SCD compared with medications (64%,),  ineffectiveness of medications (64%), and adverse reactions to medications (56%). 

Listen to this Healthlink Special: Specific Carbohydrate Diet.  Dr. Suskind explains that dietary therapy changes what the immune system reacts to… removing gut irritating food changes the gut microbiome. One mom says, “It doesn’t take much more time than cooking for anyone else, ONCE you learn the How-Tos… [for my child to] have the power and strength to keep herself healthy and in remission without relying on medications is the greatest gift I can give her.”   Another child says, ” I GO out to eat; I GO out with friends. I can usually find food I can eat no matter where I go.”  Another mom says, “I have a kid with a chronic disease that is HEALTHY, quite a paradox!” 

I encourage the IBD families I make aware of the microbiome and SCD to travel and become patients of children’s hospital affiliated GI clinics which have integrated SCD into IBD clinic therapeutics across the US such as Dr. Suskind at Seattle Children’s, Washington State.  For most, their primary GI physician remains local.  I can tell you, these children have gone from fecal protectin levels of 400+ at time of diagnosis, to 200s within weeks of beginning SCD, to under 100 within months of eating SCD.  Symptoms resolve within a week for many, and lab inflammatory biomarkers normalize quickly.

What’s up with mostly only the educated knowing about SCD for IBD, AND when do we cross the threshold for legal liability for NOT offering effective SCD dietary therapy for IBD?

The [Kakodkar et al.a 50 cohort, 2015] found that 49 of the 50 SCD eaters all had college or graduate school degrees!   Why?  To implement SCD most people need to read a lot, including the PubMed studies, and learn on their own How-To eat SCD since few IBD centers add SCD into dietary therapeutics.  Dr. Suskind, [Suskind Dietary Treatment  YouTube, 2016] stresses that adequate support of SCD, including the community of those using SCD, is absolutely necessary for best patient success using SCD.

Practically, implementing SCD is not difficult once learned.  It is learning SCD however that is hard because only a few clinics integrate true support of SCD into IBD dietary therapeutics.  Most clinics only offer lame uneducated and unhelpful How-To’s if they even mention SCD at all to the patient.

For comparable, at Dr. Suskind’s clinic, the RD teaching SCD has personally eaten SCD for over three years!  It has always been a goal of mine to make practical How-to knowledge of SCD accessible to everyone.  Hopefully through efforts of the clinics therapeutically integrating SCD into IBD dietary therapy along with the microbiome researchers, knowledge of SCD will rise to the level where the standard of care legally requires physicians to disclose and integrate SCD into clinical therapeutics.  Dr. Suskind guessed that clincial integration of SCD was still 5 years away. [Suskind Dietary Treatment  YouTube, 2016]  Personally, I wonder (putting on my attorney’s hat) if it isn’t already there and actionable for nondisclosure.  UMass is amazing; UMass, has even begun teaching the IBD-AID evidence based diet cooking class and  you can read about that in this post, it is the second study listed under the lightbulb or “IBD Studies” section.

Dr. Sandra Kim 2014 presentation: “Probiotics, Special Diets, and Complementary Therapies: We Know Patients Want Them, so What do We Tell Them?

Last, I link to the 2014 Power Point presentation by Dr. Sandra C. Kim, MD, titled “Probiotics, Special Diets, and Complementary Therapies: We Know Patients Want Them, so What do We Tell Them?”   This presentation was given at the annual 2014 Advances in Inflammatory Bowel Diseases, Crohn’s & Colitis Foundation’s Clinical and Research Conference.  Dr. Kim talks about two SCD and IBD clinic studies, [Cohen et al. 2014] and [Suskind et al. 2014] and notes that there is significant disease activity indices improvement and endoscopic or mucosal healing happening for IBD patients eating SCD. Dr. Kim further notes, “…certainly there is some promise in at least thinking about this.”  See time 15:35.  As well, at time 18:31, Dr. Kim recommends specifically being proactive, open, and ask patients about CAM interests and usage.  I especially appreciate that Dr. Kim notes that being current in the literature is absolutely necessary so as to not lose credibility.  Recently, Dr. Kim was appointed co-director of the Inflammatory Bowel Disease Center, a Division of Pediatric Gastroenterology, Hepatology, and Nutrition at Children’s Hospital of Pittsburgh, but this group does not offer support of SCD for IBD!

Conclusion

I wrote this post to try to put in one place, the summary of studies conducted to date on the SCD.  It focuses on SCD for IBD because that is where most of the studies are happening.  Whatever your disease concern, try the tenets of SCD.  Diet changes the microbiome which changes the immune status.  You truly have everything to gain health wise.

The references used in this post, as well as the seventeen that came up on a PubMed search for “Specific Carbohydrate Diet,” are listed below my signature.

The microbiome studies and clinics integrating SCD for IBD are showing that SCD changes the gut microbiome and can induce remission for IBD without medications for many with mild to moderate IBD. For those with failure of medications, SCD can help the medication efficacy which is important to stave off surgical intervention which removes diseased intestine.  About half the patient population turns to SCD due to hesitation of medications as they have  great risks.  The other half turns to SCD due to failure of the medications to induce IBD remission.  Medications can’t modulate the inflammatory microbiome when you keep ingesting irritating foods.

Best in health through awareness,

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♥  to add the many other versions of SCD now in study.: You’ll even see that modified versions of SCD are also in study for IBD like PRODUCE, CDED, CD-TREAT, IBD-AID, Low FODMAP, Mediterranean! [Sabino et al 2019].” Figure 1 from this study was also added.
Prior update Feb 28, 2018 added “Make sure you look at the comments below this post for even more links to studies that have published since I released this post.”  Also, Suskind, et al, 2016 (which published online) was updated to link to the full text which published in J Clin Gastroenterol, 2018 Feb; 52(2): 155–163, for “Clinical and Fecal Microbial Changes With Diet Therapy in Active Inflammatory Bowel Disease.” The prior update April 22, 2017 added that the Nutritional Adequacy of SCD is confirmed and explained by Dr. Suskind’s RD, Kimberly Braly in this April 9, 2016 presentation.
References I cited above, in order of appearance:

[Sabino et al 2019] Treating Inflammatory Bowel Disease With Diet: A Taste Test, https://www.gastrojournal.org/article/S0016-5085(19)41036-6/pdf

Suskind et al., 2016, Patients Perceive Clinical Benefit with the Specific Carbohydrate Diet for Inflammatory Bowel Disease.  417 survey (online) of SCD Web sites and support groups in an attempt to characterize patient utilization of the SCD and perception of efficacy of the SCD.   47% had Crohn’s disease, 43% had ulcerative colitis, and 10% had indeterminate colitis. Individuals perceived clinical improvement on the SCD. 4% reported clinical remission prior to the SCD, while 33% reported remission at 2 months after initiation of the SCD, and 42% at both 6 and 12 months. For those reporting clinical remission, 13% reported time to achieve remission of less than 2 weeks, 17% reported 2 weeks to a month, 36% reported 1–3 months, and 34% reported greater than 3 months. For individuals who reported reaching remission, 47% of individuals reported associated improvement in abnormal laboratory values.

Click here to read full article

Defy Autoimmune Psoriasis: Green Tea, Black Tea, Lemon Juice Antioxidant

SUMMARY:  Plenty of studies find anti-inflammatory effects of dietary antioxidants such as green tea for chronic disease.  Even in IBD patients, who have a very messed up microbiome (a finding of the American Gut data), the  benefits of antioxidant therapy is well documented (see below studies).  Read here about a simple EASY N=1 hack for one IBD patient that shut down a mild psoriasis skin flare that began two years ago.  They flared psoriasis, but not the autoimmune IBD, eating strict healing diet Specific Carbohydrate Diet (SCD) probably due to a gluten/sugar airborne exposure.  The hack that worked for stopping psoriasis: Green Tea, Black Tea with Lemon Juice antioxidant blend!  I share their recipe here!   It is simple enough that you may want to add it to your immune calming anti-inflammatory arsenal too!  Make sure to see below for why it is important to NOT drink Green Tea for antioxidant benefit along with Iron.  

If the tea and lemon juice blend posted here isn’t your cup of tea, try extending the concept and increase other antioxidants.  For ideas, see below for the

Phytonutrients from Dana Farber Brigham and Women’s Cancer Center PDF

Click here to read full article

Microbiome, Emulsifiers, IBD & Metabolic Syndrome

SUMMARY: Don’t be duped into believing diet has nothing to do with your disease, or in preventing disease.  When the researchers themselves rethink and change up their own diet to eliminate the ubiquitous food additive emulsifiers because their research is finding serious adverse impact on the gut lining, I want everyone to rethink their emulsifier intake too, for your gut’s health.  Meet here, Dr. Andrew Gewirtz  and learn about his important work on Microbiome, Emulsifiers, and their association with IBD and Metabolic Syndrome (defined by NIH as having three or more of these factors or you take drugs to control them:  High triglyceride level, reduced high-density lipoprotein (HDL) cholesterol, increased blood pressure, elevated fasting blood sugar, & large waist circumference.  How concerned should you be about chowing down emulsifiers?  Their connection to gut inflammation and microbiome skew at the mucosal level caused Dr. Gewirtz to eliminate such from his and his family’s diet.  One tenet of the healing diets — eliminate processed foods — results in the elimination of emulsifiers. Perhaps it is time to reconsider your emulsifier intake too.

WHY ELIMINATE EMULSIFIERS?

Andrew Gewirtz’s studies in mice show that it is a matter of microbiome and microbes when it comes to emulsifiers in the diet.

lightbulb2Feeding mice emulsifiers altered the microbiota microbiome and Gerwirtz found, for mice, they got:
  • IBD (for mice with predisposition to this disease), and
  • Low-grade or mild intestinal inflammation and metabolic syndrome for mice having normal immune systems.  Metabolic syndrome is characterized by increased levels of food consumption,  diabetes, hyperglycemia, elevated cholesterol, elevated triglycerides. insulin resistance, and obesity. This work supports earlier findings that low-grade inflammation resulting from an altered microbiota can be an underlying cause of excess eating.
  • What’s metabolic syndrome?  The National Institutes of Health guidelines diagnose metabolic syndrome if you have three or more of these traits or are taking medication to control them:
    • Large waist circumference — a waistline that measures at least 35 inches (89 centimeters) for women and 40 inches (102 centimeters) for men,
    • High triglyceride level — 150 milligrams per deciliter,(mg/dL), or 1.7 millimoles per liter (mmol/L), or higher of this type of fat found in blood,
    • Reduced high-density lipoprotein (HDL) cholesterol — less than 40 mg/dL (1.04 mmol/L) in men or less than 50 mg/dL (1.3 mmol/L) in women of this “good” cholesterol,
    • Increased blood pressure — 130/85 millimeters of mercury (mm Hg) or higher,
    • Elevated fasting blood sugar — 100 mg/dL (5.6 mmol/L) or higher.

    Gerwirtz’s study suggests that the current means of testing and approval of food additives may not be adequate to prevent use of chemicals that promote diseases driven by low-grade inflammation and/or which will cause disease primarily in susceptible hosts. Actually though, you know by now that low grade inflammation is synonymous with many diseases, and many diseases have signature microbiomes.  If you don’t —  check out the drop down menu over on the right side bar to see your disease of interest.

    Next up for Gewirtz’s animal microbiome emulsifiers findings — these studies are now being extended to human trials led by researcher Dr. Gary Wu, University of  Pennsylvania

    I am looking forward to the human data.   A simulation of emulsifiers in the human gut performed in Belgium has confirmed the inflammation increase observed in the mice.  If similar results are obtained in the human trials, such would indicate that emulsifiers play a role in driving the epidemic of obesity, its inter-related consequences and a range of diseases associated with chronic gut inflammation.

    Microbiome dysbiosis cause and effect at this time is not clear. Dysbiosis might cause disease as researchers learn more about how the microbiota can influence the host, but diseased states can also lead to changes to the microbiota. Some mechanisms include the addition of medications such as antibiotics as well as microbiome changes resulting from eating habits [think about the emulsifier additives discussed in this post] and bowel function [IBS, SIBO…]. -The gut microbiome in health and in disease, 2016

    New restrictions on common ubiquitous emulsifiers would require food processors to scramble for alternatives to maintain  texture, appearance, and quality of their foods and beverages; or we get use to understanding what real unadulterated food is supposed to look like… we learn to stir our peanut butter…  This is beginning to sound similar to the death knell of trans-fat elimination from countless products.

    What are emulsifiers?

    Gerwirtz explains:  Emulsifiers are a common class of food additives in virtually all processed food.  Many are chemicals, and many are synthetic meaning they do not exist in nature such as carboxomethylcellous and polysorbate 80 .  They improve texture but mainly their main role is to increase shelf life.  Emulsifiers stabilize mixtures (prevents ice crystals for ice cream, keeps cookies or bread soft, salad dressings and other liquids stay blended that otherwise would separate, etc… ) and they are detergents.  -Gewirtz interview, the American Microbiome Institute, Episode 3:Emulsifiers in our food with Dr. Andrew Gewirtz, March 2015.  Actually, emulsifiers are only one type of food additive; for a complete listing of emulsifiers see the Code of Federal Regulations, Title 21.

    Many components in the food system instigate gut inflammation  

    Diseases such as rheumatoid arthritis (25), colorectal cancer (26), obesity (27), and diabetes (28) as well as cardiovascular disease, IBS, IBD, Clostridium difficile infection have now been associated with microbiome skew.  

    It only makes sense to look at your diet and rethink those dietary components now known to cause gut inflammation.  Some components of diet found associated with gut inflammation in susceptible animal models was summarized in the study, Reciprocal Interaction of Diet and Microbiome in Inflammatory Bowel Diseases.  Such included certain types of higher fat (palm, soy and other fats are discussed here — PUFA Omega-6 corn oil was used in this researcher’s work, see full text study here), as well as the Gerwirtz emulsifier studies (the focus of this post), and the artificial sweetener studies.  Most all of these can be reasonably eliminated and substituted with anti-inflammatory choices.  You can read about the soybean oil, vegetable oil, and corn oil connection to diabetes and metabolic syndrome here.  The type of fat consumed and the connection to breast cancer diagnosis can be read here. The conclusions of those posts is that until the dust settles on fat types and disease… just use oils having long term non controverted known benefit such as EVOO (be certain it is not adulterated with the soybean, corn and vegetable oils — see those posts for listings).

    lightbulb2

    Gut inflammatory food substrates are so ubiquitous in today’s food system that It has come to the point that label reading, though it takes time, is worthwhile.  Decrease inflammatory instigation in the gut by choosing foods containing ingredients so that you know what they are.  

    lightbulb2

    Eating out at restaurants?  Why would you drop $20/meal to eat a lot of ingredients that are going to inflame your gut?  Choose raw produce for salads including avocado and hard boiled eggs, bring your own EVOO salad based dressing, and tell them to cook your meat/fish using only EVOO.  Update:  I did not include chicken.  Why? Most have non-SCD broth injection.  You can go so far as to bring your own seasonings and sea salt to eliminate the anti-clumping additives of their spice blends and spice powders such as garlic powder and onion powder.

    Click here to read full article

Finally, an IBD microbiome drug goes to clinical trial

Summary:  Seres Therapeutics began its Phase 1b placebo controlled clinical trial on Dec 14, 2015, for SER-287, which is the first drug aimed at the microbiome for a non-infectious, chronic condition, ulcerative colitis (UC).  This is the first IBD microbiome drug that actually targets the constituents of the microbiome. This approach treats chronic disease without suppressing  the body’s immune response. Instead, specific strains of bacteria are introduced that re-balance the billions of different types of bacteria that are in the digestive tract, which then increases immunity and manages the disease.  Instead of being immunosuppressive, this treatment targets the root cause of UC  which is gut dysbiosis, increasing immunity. SER-287 clinical trial is currently recruiting participants if you are interested; contact information is below.

Note:  The immune system outsmarts anti-TNF meds a lot of times — 30 to 80% of the time for IBD.  Isn’t that a crazy broad failure range?  This post speaks to some of the whys of that failure.  And… realize a lot more diseases use these immunosuppressive meds beyond IBD.

I wrote about the immunosuppressant and biologic microbiomes not looking ‘healthy’ in this post, and in fact had the opportunity to have that very question answered and confirmed by Johns Hopkins GI expert Dr. Gerard Mullin, MD at the Evolution of Health Functional Forum, called Microbiome Maximized Medicine, held in NY on October 5, 2015.  The YouTube of that dialogue can be linked to on this post.

These disease microbiome drugs are not immunosuppressive, rather their mechanism of action is to enhance and increase immunity.

Incidentally, healing diets also introduces microorganisms and food substrate matter into the gut that cause mucosal healing with increased immunity to manage chronic disease

I wrote about the microorganisms we ingest at: AVG NUMBERS AND KINDS OF MICROORGANISMS CONSUMED IN A DAY.  Interestingly, the USDA dietary pattern had the highest total microorganisms for the day, due to yogurt and cottage cheese consumption, whereas the AMERICAN and VEGAN dietary patterns had 3 orders of magnitude fewer total microorganisms primarily due to heating probiotic type food such as cheese (which kills microorganisms) or the diet lacks consumption of probiotic type foods.  I am certain the FODMAP type foods omitted or ingested also impact microbiome richness since these food substrates are food for bacteria which if provided, will accordingly bloom bacteria. See here for a FODMAP post. Healing diets contain unheated live fermented foods and tolerable FODMAPS and have been shown to increase microbiome diversity and immunity in compromised guts.  See this post for IBD: 50 IBD SCD REMISSION PATIENTS: RUSH PAPER.

“Bugs as drugs” idea for disease treatment

Startups are harnessing the trillions of bacteria inside us to eradicate chronic disease such as diabetes, obesity, arthritis, MS, autism, depression, and more. This “bugs as drugs” idea for disease treatment packages live strains of bacteria originating from a healthy donor’s microbiome to be used as therapy.

This all began as a fecal microbial transplant (FMT) which is currently approved for antibiotic resistant CDiff infection and has over 90 percent cure.  A startup that  provides FMT substrate matter originated out of a not-for-profit from MIT and is called OpenBiome.  Mark Smith is OpenBiome’s founder who considers that the oral application wouldn’t just reduce the discomfort of the FMT transplant, but that “swallowing a capsule of someone else’s healthy digested material — [that’s where the live strains of bacteria are coming from] or eventually swallowing strains cultivated in a lab,—could become a maintenance therapy for sufferers of a variety of gastrointestinal disorders, and for that, “We’re in the testing and evaluation phase.”  Side bar:  Anecdotal evidence from my follow of numerous DIY groups does lean towards needing repeat FMT for some diseases. Diet impact post-FMT microbiome is not well understood (nor is it understood pre-FMT for the donor) which could impact acceptance of the transplanted microbiome sooner.

FMT are not the way of the future. They are just a transitional solution… [for OpenBiome’s capsule, the first patient to test will be] a quadruple amputee with C. diff. She’s not a good candidate for a fecal transplant, but her doctor thinks this pill might be perfect.” MIT Lab Hosts Nation’s First Stool Bank, But Will It Survive? and WHAT’S LURKING IN YOUR MICROBIOME? POSSIBLY, A CURE FOR DISEASE

Why start with IBD for “bugs as drugs”?

The short of it is, they are picking diseases with known causation being gut dysbiosis; there is a difference with correlation and causation.  “If you’re going to leverage the microbiome for drug discovery, it’s not the correlations that matter. It’s the causal relationships. How are the bacteria interacting with the host in a way that’s driving our biology? Did patients with bowel or intestinal diseases—colitis, for instance—have different gut bacteria profiles because they were ill? Or were they ill because they had different gut bacteria profiles? For example, children with autism often have significant gastrointestinal problems. Yet is that a reason for their autism, or is it just a related fact?”    -WHAT’S LURKING IN YOUR MICROBIOME? POSSIBLY, A CURE FOR DISEASE

The diseases in the right quadrant represent those with known causation as microbiome dysbiosis. Left quadrant diseases have been associated with gut dysbiosis.  DiLaura, of Second Genome, explains, “So our efforts, right now… aims to create a drug for IBD. Difficult as that sounds, it is a modest goal compared to the company’s second order of business: create a drug for metabolic diseases like type 2 diabetes. The first drug, if effective, could affect hundreds of thousands of people; the second, millions”. -WHAT’S LURKING IN YOUR MICROBIOME? POSSIBLY, A CURE FOR DISEASE

Background on Seres medicines

All of Seres’ medicines are made up of  biologically-sourced bacterial spores (which are very different from fungal spores) which can be collected in a capsule for easy administration.  

The first drug candidate from Seres to reach clinical trials is for treatment of Clostridium difficile infection (CDI) in adults; this drug. SER-109, is now in Phase 2 trials and is a mixture of bacterial spores from 50 bacterial species taken from healthy donors.  Currently, FMT is used to treat recurrent antibiotic resistant CDI with over 90 percent cure.

SER-287 is the second Seres drug joining alternative capsule treatment for FMT but this time for UC. SER-287 is a microbial cocktail capsule containing “a complex and diverse bacterial spore ecology.

I am concluding the specific microbial composition of SER-287 is sourced from healthy donors as is SER-109; the trial is looking at engraftment of SER-287 bacteria into the intestinal microbial community. Ordinarily, commercial probiotic bacteria such as in yogurt, does not engraft into the microbiome.  These bacteria are transient and repeated consumption is required to maintain and sustain benefit.  Benefit often ceases about 3 days post consumption.

If you want further detail on Seres, see Seres therapeutics website.

Clinical Trial details for SER-287, the first IBD microbiome drug that targets the microbiome

The link to the study is: A Study to Evaluate the Safety, Tolerability and Microbiome Dynamics of SER-287 in Subjects With Ulcerative Colitis.  About 55 patients are expected to enroll; the trial is currently recruiting participants.  The drug used, SER-287, treats UC without suppressing the body’s immune response. Instead, SER-287 delivers specific strains of bacteria to re-balance the billions of different types of bacteria that are in the digestive tract, which then manages the disease.  This treatment is not immunosuppressive; instead it targets the root cause of UC which is gut dysbiosis.

The current standard of care for UC treatment uses drugs that suppress the immune system to reduce inflammation in the colon and rectum which makes patients susceptible not only to infectious diseases, but to cancers that would otherwise be killed off by the immune system.

Primary Outcome Measures of the Clinical Trial:
  • Safety and tolerability of SER-287 vs. placebo in adult subjects by analysis of AE’s, lab values, vital sign, physical exam findings, medical history, and ECG.
  • Examination of baseline composition of the intestinal microbiome to the composition. Changes in the composition of the microbiome will be characterized by rDNA 16S V4 genomic data sets. Changes will be assessed by total number of unique bacteria and microbial composition.
  • Engraftment of SER-287 bacteria into the intestinal microbial community. Microbiome will be characterized by rDNA 16S v4 Genomic Data Sets. Engraftment will be assessed as the outgrowth of bacteria that compromise the SER-287 spore ecology in the subjects GI tract post treatment.
The time frame for the study

December 2015 to June 2017.

Contact for the study

Michele Trucksis, PhD, MD at  clinicalstudies@serestherapeutics.com

Study Locations are:
  • United States, Florida.  Advanced Gastroenterology Ctr, Port Orange, Florida, United States, 32127.  Contact: AMMAR HEMAIDEN, MD    386-763-4920
  • United States, Maryland. Capital Digestive Care, LLC – Metropolitan Gastroenterology  Group (MGG), Chevy Chase, Maryland, United States, 20815. Contact: ROBERT HARDI, MD    240-737-0085.
  • United States, Massachusetts. Community Clinical Research Network, Marlborough, Massachusetts, United States, 01752. Contact: JOHN CURRAN, MD    508-320-9248
You can read more about Seres and SER-287 here:

CEO: Seres Therapeutics ‘walks into flying’ with new trial in ulcerative colitis:

As to why they are targeting UC and not a larger population affected condition such as Type 2 Diabetes or Metabolic Syndrome:  Pomerantz, CEO of Seres explained, “As someone who’s worked on eight infectious disease drugs, I know that you want to walk into flying. You don’t want to fly into flying.”  Seres intends to target metabolic diseases in addition to inflammatory and infectious ones, but other recent microbiome startups are looking even further, at fields like autism or others. Pomerantz maintains that while such diseases may be in the realm of those which can be treated by rebalancing the microbiome, “we don’t think that was smart” to start with them.

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Do microbiomes on drugs look healthy? Biologics & PPI

Summary:  I’ve wondered literally for years now, ever since I first learned of the microbiome, do microbiomes on drugs look healthy?  I call it the “drugged microbiome,” and I (foolishly perhaps) expect the drugged microbiome to look like a “healthy microbiome”  since this is where 80 to 85% of our immune status resides.  We already know that ~60 drugs are known to be affected by the microbiome  though researchers suspect the real number is much higher.  My question turns this on it’s head and asks, 

“What’s your drug doing to your microbiome?”

Though this question applies to any and all drugs, this post looks at immunosuppressants/biologics and proton pump inhibitor (PPIs)  mainly since there is a lot of published insights into what the drugged physiology and microbiome looks like as well as user health status. Also, a lot of folks use these drugs or they are a top in sales.  From April 2014 through March 2015, PPIs esomeprazole (Nexium, AstraZeneca) ranked third in number of prescriptions written having ~18.2 million and biologics Humira (adalimumab) was the number 1 top sales drug at $8.2 billion with Remicade (infliximab) ranked tenth in sales at $4.6 billion 

lightbulbYou can investigate your particular medication microbiome impact by goggling your disease’s name, microbiome, and diet.  Pay attention to PubMed and journal results.  Tease apart the study cohort to learn the reference microbiome.  If the microbiome diversity is increased using diet, the drug likely is not nudging the microbiome to health. Use the same logic as the meds examined herein.

Spoiler alert: It seems immunosuppressant and biologic microbiomes are not ‘healthy looking’ as altering such with diet increases it’s diversity, nudging it towards more healthy, and can even result in reduction and/or elimination of the meds. The PPI microbiome is not healthy, and it is wrought with devastating health risks.  Many use PPIs without indication based evidence including nearly half of nursing home patients. 

Clearly, modern medicine is not tracking modern science

I don’t want pharma hate mail but it’s time all drug users question and know what the drug is doing to their microbiome.  If the host’s microbiome remains in dysbiosis, that is strong evidence (putting on my attorney and mechanical engineer hat) that the drug is acting on only symptom suppression and not restoring microbiome health and immune status. Immunity is still compromised opening doors for disease relapse or pulling the trigger for other chronic disease(s). Sooner or later, that inflammation is going to get you.  

Ironically, symptom resolution instead of microbiome health may be what Pharma wants

Pharma now appreciates that their product feeds the microbiome playing a huge role in drug metabolism, activation and reactivation. This paper notes that specific enzyme targets in the microbiota can be potently and selectively disrupted to achieve clinical outcomes… components of the microbiome should be considered “druggable targets.”  

This paper, The Gastrointestinal Microbiota as a Site for the Biotransformation of Drugsclarifies with a cautionary note:

The microbiota secrete a diverse array of enzymes (primarily for carbohydrate and protein fermentation) giving them substantial metabolic potential which can have major implications for drug stability. At least thirty drugs which are, or have been, available commercially, were subsequently shown to be substrates for these bacterial enzymes, and with increasing numbers of new and existing drugs having the potential for contact with the distal gut (through modified release systems or poor solubility/permeability), many more are expected to be discovered. The major concern with bacterial drug degradation is the behaviour of the metabolite; is it more or less active than the parent compound, or has toxicity resulted? For example, there were eighteen deaths in 1993 due to a drug interaction in which a toxic drug metabolite was produced by bacterial fermentation.

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SCD thoughts given DrOz 3 Day Cleanse, Microbiome

SUMMARY:  Finally! A peek into our trillions of innards on a 3 day fruit and vegetable blitz!  Spoiler alert:  There is NOT much impact 10 days after stopping that 3 day cleanse, microbiome resulting from healing diet tenets persist!  

And that, I think, is the lesson to be learned for the healing diets such as SCD, GAPS, PALEO, AIP, WAHLs, to name a few.  Realize, the tenets of these healing diets are for everyone if you want to prevent chronic disease, not just those with chronic disease.  These protocols increase vegetables and fruits beyond what the normal Standard American Diet (SAD) yokel is consuming and adds in healthy fats so fat soluble vitamins are actually absorbed.  This is done concomitant with ditching processed foods,  including processed sugars, and other inflammatory foods.  How powerful are these tenets?  They are healing and inducing remission in messed up impoverished gut microbiomes, and some of those folks are only 80% compliant with the diet!  Nuff said.  Shouldn’t you know what these tenets are?

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