Last Updated on February 18, 2017 by Patricia Carter

SUMMARY:  Anytime food choices turns around chronic disease with studies that prove such, that should be an eye opener!  Implementing principles of such diets should be considered for anyone wanting to prevent or manage chronic disease.  This post presents studies for Food Managing IBD & AUTISM, where dietary protocols achieved remission and management (with reduction, if not elimination of medication) for autoimmune IBD , or positively altered the course of autism.

HOW?  Diet can optimize (or modulate) the gut microbiome which is the source of 80 – 85 percent of our immunity:  

The “1st International Symposium on the Microbiome in Health and Disease with a Special Focus on Autism,” July 2014: “the microbiome refers to the constellation of enteric bacteria that create an organ system that makes up 80% of our immune system...“

So too does  Natasha Campbell-McBride, MD, noting multiple times “85% of the body’s immune system can be found in the gut,“ (see here),   Her book,  “Gut and Psychology Syndrome,”   is followed by countless numbers managing autism thorough the GAPS diet which is based on SCD.  Her bio: MD, Master of Medical Sciences in Neurology and Master of Medical Sciences in Human Nutrition.

More on the “1st International Symposium on the Microbiome in Health and Disease with a Special Focus on Autism,” July 2014: “the microbiome refers to the constellation of enteric bacteria that create an organ system that makes up 80% of our immune system...  Scientists are diligently working to understand how xenobacteria and commensual bacteria communicate and interact to influence health and how alterations in populations of bacterial species may alter host health and contribute to chronic disease. “  The goals of this incredible conference are to:  “bring together a world renowned group of experts to present their work on the microbiome in health and disease with a special focus on Autism. Researchers hope to consolidate this information into a formative discussion aimed at designing a clinical trial that can elucidate pathophysiological mechanisms related to the microbiome in Autism and possibly promote new treatment strategies to address core underlying biological alterations through targeted treatment approaches aimed at manipulating the microbiome.”  Further details of this conference are discussed below in the “AUTISM AND IBD MICROBIOME SHIFTS ARE NOW INDISPUTABLE“ Section. 

Still wondering about this huge 80 to 85% gut immunity rate?  Watch this video presentation to appreciate the role of your gut mucosa, which is the largest and most dynamic immunological environment of the body.  Realize we now know that many diseases have altered microbiomes, not just the focus of this post (IBD and autism). 

You’ve discovered the key cells and molecular players involved in gut immunohomeostasis and disease: the crypts, Tcells, dendritic cells (regulators of innate and adaptive immunity by acquiring, processing, and presenting antigens to T cells), antigens, tolerogenic activation (tolerogenic cells induce regulatory Tcells), anti-inflammatory response, Tregs (specialized T cells that exert immunosuppressive function), IL-10, tumor necrosis factor, and neutraphils just to name a few!

WHY AM I HIGHLIGHTING AUTISM AND IBD FOOD STUDIES?

First, MANY are affected and MANY are children that are put on medications (usually lifelong).  That actually is a double whammy considering the fetal impact due to drug exposure once these children reach child-bearing age.  SCD (and GAPS which is based on SCD) heals the gut and studies presented below support medication reduction and/or medication elimination. 

Second, any parent would want to know that dietary options exist to manage such.  Interestingly, it is well known that a high prevalence of food sensitivities exist in Crohn’s Disease patients, and enteral nutrition is not only the first-line of therapy in Japan,  but a known research method used to place the majority of Crohn’s patients into remission.  Lastly, I should note, the legal system precludes your doctor from sharing diet alternatives since this is not the legal “standard of care” which your doctor must adhere to.  Ok… I’m done wearing my attorney hat.

AUTISM PREVALENCE:  In 2014, the prevalence of autism is 1 in 68 (1:68).  That is a 30% increase from two years ago, and thirty years ago it was 1:10,000.  The increasing prevalence since the year 2000, as cited in this article, is alarming:

1 in 68 is 6.5 million American children, 11 percent of school age.   And the increases are not due to increasing ability to diagnose, Cynthia Nevison’s paper: “between 75-80% “of the tracked increase in autism since 1988 is due to an actual increase in the disorder rather than to changing diagnostic criteria“.   Add on to that, 2/3 of them are receiving mind-altering medications.  And, to add on even more to that, appreciate that 90 percent of ADHD drugs (ADHD and autism lines blur) sold are to Americans, yet we only constitute 5 percent of the world’s population.  Not surprising that what we eat can affect these conditions (and other chronic disease) if you are followers of my work.

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IBD Prevalence:  IBD, according to the CDC, is a childrens disease with peak age at onset being 15 – 30 years, although 10% of cases occur in individuals younger than 18 years.  Precise incidence and prevalence of IBD (Crohn’s disease and ulcerative colitis) have been limited by (1) a lack of gold standard criteria for diagnosis; (2) inconsistent case ascertainment; and (3) disease misclassification.  It is estimated that as many as 1.4 million persons in the US suffer from IBD;  it is one of the five most prevalent gastrointestinal disease burdens in the US with an overall health care cost of more than $1.7 billion. This chronic condition is without a medical cure and commonly requires a lifetime of care. Each year in the US, IBD accounts for more than 700,000 physician visits, 100,000 hospitalizations, and disability in 119,000 patients. Over the long term, up to 75% of patients with Crohn’s and 25% of those with UC will require surgery. 

Dr. Cheifetz, Adam S., MD,  Director, Center for Inflammatory Bowel Disease at Beth Israel Deaconess Medical Center, Boston, MA, similarly noted statistics in JAMA as:

Dr. Ece Mutlu’s article (she is a primary investigator of SCD for IBD having interests:  Diet therapy in Inflammatory Bowel Disease, Role of microbiological flora on gastrointestinal illness, Role of nutrition in gastrointestinal disease, and Complementary and alternative medicine for gastrointestinal disease) explains:

“[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”, Expert Review of Gastroenterology & Hepatology, Informa Healthcare.

AUTISM AND IBD MICROBIOME SHIFTS ARE NOW INDISPUTABLE:

This 2013 PLOS ONE study: “Reduced Incidence of Prevotella and Other Fermenters in Intestinal Microflora of Autistic Children” showed that “autism is closely associated with a distinct gut microflora that can be characterized by reduced richness and diversity as well as by altered composition and structure of microbial community. The genera Prevotella, Coprococcus, and unclassified Veillonellaceae were significantly reduced in autistic children. Unexpectedly, these microbial changes were more closely linked to the presence of autistic symptoms rather than to the severity of GI symptoms and specific diet/supplement regimens. Despite limited information on the direction of causality among autism, diet, GI problems, and microbiome profiles, the findings from this study are stepping stones for better understanding of the crosstalk between gut microbiota and autism, which may provide potential targets for diagnosis or treatment of neurological as well as GI symptoms in autistic children.”

This 2014 YouTube: “The Potential Role of Gut Microbes To Correct Microbiome Imbalance in Autism,” presented at the 2014 annual meeting of the American Society for Microbiology, provides more evidence that bacteria in the gut is linked to autism.  Both Dae Wook Kang, Arizona State University and Lita Proctor, National Human Genome Research Institute, NIH, discuss the potential role of gut microbes, diet, and autism.  Proctor says, “We are redefining what a pathogen is (disease causing bacterium)… we need to add the microbiome imbalance causes pathogenic behavior (disease causing).”

http://www.youtube.com/watch?v=uQ2lU6MvVYU&list=PLD2Sv5NskYtyM7qVvXGv1JeyYp7frE3nw#t=60

Kang et al found that children with autism have significantly different concentrations for 7 of the 50 compounds they identified, of certain bacterial-produced chemicals, called metabolites, in their feces compared to children without ASD.  “Most of the seven metabolites could play a role in the brain, working as neurotransmitters or controlling neurotransmitter biosynthesis,” says Kang.  “We suspect that gut microbes may alter levels of neurotransmitter-related metabolites affecting gut-to-brain communication and/or altering brain function… Gut microorganisms are thought to play a major role in the brain, affecting mood, anxiety, and pain.  Now we are seeing they may play a role in development as well.”

 Kang became an autism researcher as the result of seed money from volunteer parents of autism.  [Wow, incredible parents!]  The significance of measuring candidate metabolites:  this is promising and would be an early biomarker of disease; none is now available; diagnosis is by symptoms only.  The community of microbiome determines the metabolites.  Ten years ago the technology was not able to see the large amount of metabolites crossing over microbiota and affecting humans.  Antibody profiles may be a possible bio-marker too.  Want to see how metabolites change with altered diet.  Warranted for future study.  Microbiome makes metabolites that may change human  behavior.   This podcast is so important that I added my notes from the view of this podcast at the very bottom of this post under my signature for those interested.

NINE more 2014 state of the art AUSTISM MICROBIOME SKEW RESEARCH (and other information can be gleamed from: “1st International Symposium on the Microbiome in Health and Disease with a Special Focus on Autism,” July 2014 with speakers: Frye and here for his presentation (Mitrochondrial dsyfunction), Parker (fauna and flora), Allen-Vercoe (Canadian fermentation machine – microbiome is the forgotten hero), MacFabe (bacteria metabolites are possible autism triggers), Adams (gut bacteria), Midtredt (gut and brain), Swedo (OCD), Cerneglia (antimicrobial residues in food), Krajmalnik-Brown (gut bacteria)… Those names should strike a cord if you are at all into autism research; otherwise, get listening.

Studies of diet and autism are cutting edge.  As this article notes, researchers don’t know yet exactly how gut bacteria influences behavior:  

IBD HAS INDISPUTABLE SKEWED MICROBIOME

This study is a collaboration of USA (Harvard, MIT, and Brown University) and France (Hopital Saint-Antoine and UPMC University of Paris), 2012 documents not only the microbiome shifts for IBD but goes deeper and looks at the differences between IBD-Crohn’s, IBD-Ulcerative Colitis, AND looks at that due to the immunotherapies now used for IBD-Crohn’s.  Additionally this paper assessed the  functional consequences for the various microbiome shifts concluding: shifts had consequences in microbiome function that revolved around metabolism in the presence of oxidative stress and perturbed nutrient availability during tissue damage. The study population was: 121 had Crohn’s, 75 Ulcerative Colitis, 27 healthy controls, and 8 indeterminants which I assume means it was IBD but not able to diagnosis for certain if Crohn’s or UC.   You’ll need to read this paper at least a dozen times to figure out all the permutations, BUT, it is clear to me that in simpleton, 1) the microbiome shifts to produce more mucosa due to inflammation and functional consequences are: A) species that thrive in that environment are not friendly, and B) they reduce bacterial species that produce substances that are consumed by other species that in turn (the mega anti-inflammatory immune modulating critical compound) (see this Journal of Medical Microbiology article for much discussion on butyrate), C) anti-inflammatory bacteria are reduced (some produce butyrate directly) and D) this scenario continues to hold true even for those on the immunotherapies which is surprising.   After reading this paper more than a dozen times, and this is my opinion only, I am more convinced than ever that dietary management, and I am hoping that it works for the individual, is a necessary way to go since continuing to eat an inflammatory diet keeps the microbiome shifted no matter the treatment, and that seems like it can’t possibly be good given that butyrate, an end product, is dramatically reduced.  This paper also references a ton more studies that document microbiome shifts for IBD if you are interested.

This study is a collaboration of USA (Harvard, MIT, and Brown University) and France (Hopital Saint-Antoine and UPMC Unviersity of Paris), 2012.  I am repeating this link as the researchers assessed the microbiome for antibiotic usage concluding:  greatly reduced or “nearly absent predominantly  Clostridiales order.  Functionally this is a huge microbiome loss as they are anti-inflammatory regulating Tcell production, they consume acetate, and they produce butyrate…  Cirpofloxacin and metronidazole are typically used for the antibiotic.”  NOTE:  A lot of the study population was on antibiotic (18% of the non-immunotherapy Crohn’s and 13% of the UC).

U Mass, Dr. Ramnik J. Xavier, MD is the senior author for this study published in Cell Host & Microbe: “The Treatment-Naive Microbiome in New-Onset Crohn’s Disease,” Volume 15, Issue 3, p382–392, 12 March 2014 analyzed microbiomes from multiple GI locations which were collected prior to treatment, in new-onset Crohn’s disease (CD).  Intestinal tissues were taken from 447 participants with a clear diagnosis of CD at 28 participating centers in the US and Canada. The study also included 221 control participants with noninflammatory gastrointestinal conditions.  The conclusion: “increased abundance in bacteria which include Enterobacteriaceae, Pasteurellacaea, Veillonellaceae, and Fusobacteriaceae, and decreased abundance in Erysipelotrichales, Bacteroidales, and Clostridiales, correlates strongly with disease status… [and] Microbiome comparison between CD patients with and without antibiotic exposure indicates that antibiotic use amplifies the microbial dysbiosis associated with CD.”    Read here  and this “Gastroenterology & Endoscopy News” article for more discussion on this study.  My note: Interesting that this study looked at the cohort “prior to treatment” therefore not seeming to consider antibiotic use as a “treatment.”  This is discerning given the antibiotic findings of  this 2012 study, which is discussed directly preceding this study, namely that a mega immune busting functional microbiome shift occurs due to the nearly absent  Clostridiales order.  Cirpofloxacin and metronidazole are typically used for the antibiotic, and a lot of the study population was on antibiotic (18% of the non-immunotherapy Crohn’s and 13% of the UC).  I don’t want to knock UMass however (senior author of this study) as they are actively evaluating and promoting what they call the IBD-AID diet which is based on SCD and explained in the “IBD FOOD STUDIES” section below.  They are doing this since they had so much success implementing this diet to the point of actually reducing medications for IBD participants that were very ill for a very long time.  UMass actually has cooking classes to help the patients learn how to do the IBD-AID diet.  I am not surprised to see them heavily involved in the IBD microbiome studies, just surprised to not appreciate the role of antibiotics relative to decimating microbiome.

This 2014 paper reports:  ” Several studies to date [32–34] have demonstrated reduced Firmicutes, in particular Faecalibacterium prausnitzii and Roseburia, and increased Ruminococcus and Enterobacteriaceae, especially adherent invasive Escherichia coli (AIEC), in IBD [35–45]…  

increased prevalence of Escherichia coli in the ileum of CD patients [36], and a very recent study has shown the ability of E. coli to trigger and potentiate intestinal inflammation in mouse models [46]. Despite, the association of this particular organism with
IBD and, in particular, CD, the precise role of adherent-invasive E. coli (AIEC) in the initiation or activation of IBD is not yet fully defined. However, there is evidence for upregulation of microRNAs, which reduce expression of proteins necessary for the autophagy response in intestinal cells [47]. This suggests that such infected epithelial cells are prevented from self-degradement and recycling of cell components. One theory is that AIEC strains, having the capability of adhering to and invading both intestinal epithelial cells and macrophages, can translocate across the bowel wall and continuously activate further macrophages, leading to the formulation of granulomas [36]. It is known that micro-organisms that are able to penetrate the bowel epithelial barrier and to bypass macrophage killing can trigger a powerful and long lasting inflammatory response [48,49]… 

increased Mycobacterium avium subspecies paratuberculosis (MAP) in the intestinal tissue of CD patients [50,51].
MAP has been defined as the etiology of Johne’s disease in cattle, a chronic granulomatous illness that
is clinically and pathologically similar to CD in humans [52]. 

Dr. Ece Mutlu presented this RUSH University Medical Center Study (which can also be read here) showing SCD dieters had greater intestinal bacterial diversity addition to having a differing microbiome composition compared to controls.  20  IBD (10 Crohn’s and 10 UC) patients following the SCD and 20 IBD patients (10 Crohn’s and 10 UC) not adhering to the diet were evaluated.  Some patients were receiving immunosuppressant medications.  An alternative link, where you can directly read the article is: Rush University Study Shows SCD Diet Encourages Greater Microbiome Biodiversity (self.Paleo).  “I have observed that a small number of my own IBD patients drastically improved on the SCD and achieved complete long-term mucosal healing, or were able to reduce or discontinue immunosuppressants for several years.  A longitudinal study following IBD patients before the start of the diet, and during and after the SCD, would have been much harder for us to complete, but I think this should be done going forward and it could help us learn a lot more in the future.”  The poster abstract presented (and I apologize for the quality of print but it is the best I can do) is:

RUSH Study Abstract Poster, page 1 of 2, Dec 2011

RUSH Study Abstract Poster, page 2 of 2, Dec 2011

NOW FOR THE FOOD STUDIES!!!

Autism Food Studies

My favorite researcher, Paul Whiteley, is also a member of ScanBrit, which was/is a meeting of minds between the group he works with and other research groups based in Denmark and Norway, who want to experimentally examine the question of whether a diet devoid of foods containing gluten and casein might be able to impact on the presentation of autism in children.  This post on his blog entitled “Autism and the GFCF diet: ScanBrit episode 2” speaks to what seems to be working for many autism and notes “These preliminary observations on potential best responder characteristics to a gluten- and casein-free diet for children with autism require independent replication” “That sentence, taken from a recent (pre-print) publication I was very peripherally involved in writing, is probably the most important thing to take from the paper by Lennart Pedersen and colleagues* and certainly is a message that I would be very keen to promote.”

Another Whiteley post, “Food and ADHD: lessons for autism?” is worth a read as it also pertains to autism since “we know that autism and ADHD can occur alongside each other and the association seems quite strong.  We also know that some people with autism seem to be affected by diet; whether as a consequence of co-morbid conditions such as coeliac disease or through less well-defined connections. “

In fact, Whiteley is also the author of the book “Autism: Exploring the Benefits of a Gluten- and Casein-Free Diet: A practical guide for families and professionals… “  Last, Whiteley authors two blogs: Questioning Answers is where he describes and discusses various research into autism spectrum and related conditions.  Gutness Gracious Me  is where he discusses various gastrointestinal research.  Nuff said there about how important this expert feels diet is to autism management.  

SCD and other Studies for Autism:  The Johnson Center for Child Health & Development: Research ongoing evaluations:

1. SCD in 20 children ages 2-6 years with gastrointestinal problems that have been diagnosed with autism.  Enrollment is now closed;  they will eat a SCD diet for 16 weeks (all food is provided) and blood, stool, and questionnaires will be obtained.  The contact for more information on this study is  intake@johnson-center or call 512.732.8400.
2. Performing a retrospective study of 600 children with a diagnosis of autism, ages 2-21 years, who were seen on an outpatient basis at the Nutrition Clinic at Thoughtful House Center for Children in 2009.  The will compare the intake of calories, carbohydrates, protein, fat, vitamins, and minerals from food at baseline and follow-up dietary consultations and assessments. The prevalence of dietary inadequacy of these nutrients in this patient population diagnosed with failure to thrive (FTT) will also be evaluated.  Enrollment is now closed.
3. This prospective treatment study is enrolling up to 50 children, ages 2-21 years, diagnosed with ASD with documented evidence of ileitis, colitis, and/or duodenitis, and lymphoid nodular hyperplasia.  They are evaluating the tolerability and efficacy of an Elemental Diet in the amelioration of gastrointestinal symptoms by conducting a prospective open trial of administering a nutritionally adequate elemental diet in this patient population.  They will quantify symptomatic changes in GI presentation as well as quantify anthropometric and biochemical changes.  Enrollment is now closed.
4. Assess bone mineral density status for 80 boys, ages 4-8 years, diagnosed with autism or neurotypical controls.  This study will determine if bone mineral density is correlated with: nutritional status, vitamin and mineral levels, symptomatic GI presentation, and antropometric measurements.  Enrollment is now closed.
5. Collaborating institutions include:
   • The Johnson Center for Child Health & Development : Research
   • Lawrence Livermore National Laboratory
   • NIH National Human Genome Research Institute
   • University of Arkansas
   • University of Texas – Southwestern
   • University of California – Davis/MIND Institute
   • University of California – San Diego
   • University of Kentucky
   • University of Seattle
   • Wake Forest University

IBD FOOD STUDIES 

1. This June, 2014 study: OBJECTIVE:: To prospectively evaluate clinical and mucosal responses to the specific carbohydrate diet (SCD) in children with Crohn’s disease (CD).  RESULTS:: Clinical and mucosal improvements were seen in children with Crohn’s using the SCD over 12 and 52 weeks.  Additionally, capsule endoscopy can monitor mucosal improvement in treatment trials for pediatric CD.  Further studies are critically needed to understand the mechanisms underlying SCD’s effectiveness in children with CD.   16 IBD children, who were monitored on SCD for 12 weeks:  Harvey Bradshaw significantly decreased from 3.3 + 2.0 to 0.6 + 1.3 (p = 0.007) as did Pediatric Crohn’s Disease Activity Index (21.1 + 5.9 to 7.8 + 7.1; p = 0.011). Lewis Score declined significantly from 2153 + 732 to 960 + 433 (p = 0.012).   Seven patients continued the SCD to 52 weeks with HB (0.1 + 0.4) and PCDAI (5.4 + 5.5) remaining improved (p = 0.016 and 0.027 compared to baseline) with mean LS at 1046 + 372 and 2 patients showing sustained mucosal healing. The study admission criteria required diagnosis of active Crohn’s with PCDAI ≥ 15.
2. This UMass study showed success for 24 IBD patients eating a whole foods diet which follows the guidelines of a slightly modified SCD diet — see here for Table 2, UMass IBD-AID Food Phase Chart.  Conclusion:  “The SCD 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. To make clear recommendations for its use in clinical practice, randomized trials are needed alongside strategies to improve acceptability and compliance with the IBD-AID.” – “Pilot Testing a Novel Treatment for Inflammatory Bowel Disease” by Barbara C. Olendzki, et al.
   SCD eliminates complex carbohydrates thought to provide the substrate for pro-inflammatory bacteria (refined sugar, gluten-based grains, and certain starches).  The second component of SCD involves pre and probiotic ingestion to reseed and restore an anti-inflammatory gut biome.  The UMass diet had 5 components: specific carbohydrates are allowed, ingestion of pre and probiotics, fatty acids are distinguished saturated, trans, mono, and polyunsaturated fats, ensures nutrient dense foods while optimizing absorption ensuring micronutrient sufficiency, and resolves food intolerances by adding in digestive enzymes or avoidance of intolerances such as eliminate additives, processing agents…  UMass has even begun teaching the IBD-AID evidence based diet cooking class and  a representative menu is:

   

   

   Slide source biomeonboardawareness.com

   

   Slide source biomeonboardawareness.com

   

   Slide source biomeonboardawareness.com

   

   Slide source biomeonboardawareness.com

   

   Pilot Testing a Novel Treatment for Inflammatory Bowel Disease.pdf
3. Dr. Ece Mutlu presented this RUSH University Medical Center Study (which can also be read here)  showing SCD dieters had greater intestinal bacterial diversity addition to having a differing microbiome composition compared to controls.   20  IBD (10 Crohn’s and 10 UC) patients following the SCD and 20 IBD patients (10 Crohn’s and 10 UC) not adhering to the diet were evaluated.  Some patients were receiving immunosuppressant medications.  An alternative link, where you can directly read the article is: Rush University Study Shows SCD Diet Encourages Greater Microbiome Biodiversity (self.Paleo).  “I have observed that a small number of my own IBD patients drastically improved on the SCD and achieved complete long-term mucosal healing, or were able to reduce or discontinue immunosuppressants for several years.“  This study showed that whole foods and eliminating certain carbohydrates is managing IBD by modulating and optimizing the gut microbiome.  This article by Dr. Mutlu’s shares the many effects diet has on the gut particularly altering directly immune function, dietary antigen load, gut microbiota, gut barrier function, xenobiotic load as well as promoting healing of the gut mucosa.  The conclusion is that dietary therapy has the potential to be a strong addition to the clinical armamentarium against IBD.  A longitudinal study following IBD patients before the start of the diet, and during and after the SCD, would have been much harder for us to complete, but I think this should be done going forward and it could help us learn a lot more in the future.”  

   

   

4. This Stanford SCD clinical trial induces IBD remission in an estimated 120 adult or pediatric  Crohn’s patients and then evaluates if SCD can be used to retain remission (effective 4/12 thru 7/15).
5. This Department of Pediatrics, Seattle Children’s Hospital and University of Washington, Seattle, WA paper documents 7 children with Crohn’s Disease receiving SCD and no immunosuppressive medications: all symptoms were notably resolved at a routine clinic visit 3 months after initiating the diet.  Laboratory indices included: albumin, C-reactive protein, hematocrit, and stool calprotectin, either normalized or significantly, improved during follow-up clinic visits. –  This studies name is: “Nutritional therapy in pediatric Crohn disease: the specific carbohydrate diet,” [J Pediatr Gastroenterol Nutr. 2014] – PubMed.
6. John’s Hopkins and Maryland University AND  CCFA are now beginning to incorporate SCD/PALEO requirements within the framework of IBD management.  Check out their PowerPoint presentations: Johns Hopkins “Nutrition Tips For IBD,” dated March 2013 and CCFA “Food For Thought,” dated April 2013.  This slide from the Johns Hopkins presentation depicts the 4 popular IBD diets and notes lack of evidence, however this is mainly due to lack of completed studies, although such is now ongoing:

   

7. Brigham & Women’s Hospital, MA: Dr. Joshua Korzenik, MD, Crohn’s & Colitis Center is looking for 200 IBD participants for a survey type study.  Access study at Crohnology or contact jkorzenik@partners.org

Last updated: February 18, 2017 at 9:04 am for SEO optimization.

In health and awareness,

My Summary of the ASM YouTube: “The Potential Role of Gut Microbes in Autism” May 2014, American Society of Microbiology with Kang and Proctor:

What is the role of the missing bacterial species, and how does this affect the host?  The gut is a fermenter: if you add the wrong components it is not helpful, if add the right components… the shift in microbiome occurs and disease state is heath.  So we can shift the microbiome community and go one way or the other.  Lower diversity is correlated with disease.  Are they missing the bacteria or just not eating the right diet?  Autism gluten-free, casein free helps autism. What can triggers are there for autism (ie appears sensitive to these environmental riggers):  vitamin and mineral deficiency.  More robust study needed to better understand the role of diet, why it works for some and not for others.

Autistic Spectrum Syndrome, males affected more so than females, and some children outgrow their autism.  Lots of sub-types of autism.  Perhaps autism will go the way of breast cancer sub types and have separate biomarkers.  Impaired carbohydrate digestion on transport is going on with autism even with same diet, the metabolites differ.  The very restrictive eating patterns perhaps are a cause and effect going on with microbiome.  7 of the 50 metabolites from fecal samples significantly differed for autism.  3 relate to the neurotransmitter.  Glutamine amino acid is increased, it’s a precursor to glutamate converted to gabba (balances neurotransmitter system), homovenomite and ? and protein builder in neurotransmitter.

Commenter:  Autism starts in fetal life, 1st trimester of life.  Sterile environment until birth, usually mothers vaginal flora innoculate baby at birth.  By 3 years of age the brain is matured.  Please explain the biofilm hypothesis in newborn  to age 3 years.

We don’t know if microbiome is cause of autism, or is it the effect of environment.  Very early studies.  Changes in pregnant mothers microbiome effect the outcome of the children’s microbiome. It’s generational that way, but not genetics (Darwin wise).  Book by name: Microbes and Evolution, the World that Darwin Never Saw:  30 years ago 1:10,000 and in 2014 we have 1:68 have autism; this is not genetics, it is environmental.  Environment has to be a factor.

Additionally, autistic have more ear infections so they have more early doses of many antibiotics and that changes the microbiome.  Antibiotics are another environmental factor.

South Korea’s rate is 1 in every 50 or 40 with autism.  They diagnose differently.  Yale University looked at this so hard to compare prevalence globally.

Kang became autism researcher as result of seed money from volunteer parents of autism.  [Wow, incredible parents!]  Measuring candidate metabolites:  this is promising and would be an early biomarker of disease, none is now available.  The community of microbiome determines the metabolites.  10 years ago technology not able to see the large amount of metabolites crossing over microbiota and affecting humans. Currently autism diagnosis is with symptoms.

Antibody profiles may be a possible bio-marker too.  Want to see how metabolites change with altered diet.  Warranted for future study.  Microbiome makes metabolites that may change human  behavior.   Time 27:40:  Kang discussion of this aspect [glutamate lower in blood but high in feces.   Proctor: researcher Kim Lewis NEUniv looking at gabba production by certain microbia in gut; suggestion made for Kang to work with Lewis.

Certain kinds of neurons are not there (lists some) and these affect the male fetus 5x more than female.  Does microbiota film… is that abnormal because genetic abnormality?

What influences our sensitivity to known pathogens:  Proctor: HMP Healthy Gore? Study 300 men/women 18-40 years ages: found totally free of disease across 5 major regions of human body, no immunomodulators, probiotics… there were 80 genomic signals present.  Significance: they had the capacity for punitive pathogens without coming out with disease; we need to look beyond our gut as well for disease wellness.