SUMMARY: GREAT NEWS: My Instagram @patty.carter is posting some of my gut flora supporting microbiome recipes!I will still continue to post recipes on this website (and other posts with direct links to the science) ⇔ I’m adding Instagram because it is a great work around for the Pinterest failure to post the entire description on images posted (at this time, they truncate descriptions when you view them)! Of course, continue contacting me direct for those Pinterest recipes, all of which focus on the healing diet tenets from SCD, PALEO, Mediterranean Diet, and others! The second reason for adding Instagram is that I will post practical insights for integrating microbiome support into your lifestyle effortlessly and seamlessly ⇒ like today’s Instagram post showed my Whole Foods Market food haul, and it linked to the newly published May, 2018 American Gut new findings ♥♥♥ The bottom line, for my Instagram…it is best if you follow me to get the full recipe and practical integration insights, (but you don’t need to) –> just link here @patty.carter! The balance of this website post shares what posted in my Instagram today which included my Whole Foods Market food haul, and the link to the newly published May, 2018 American Gut new findings (which continues to confirm that 30 different vegetables consumed each week is best for microbiome diversity and health) ♥♥♥
Tag Archives: biome
Town Hall Medicine Microbiome Talks
Background on Town Hall Medicine Microbiome Talks
This science based initiative shares my vision that knowledge is power. They believe that through access to credible science-backed information, you can have the knowledge you need to take steps to live a healthier life. To give you that knowledge, they gathered top scientists, researchers, clinicians and thought leaders from around the world – some of the best of the best from such respected institutions as Harvard, UCLA, University of Western Australia, University of British Columbia and University of Toronto – to share their research findings directly with you. These experts are highly respected in their fields, and I’ve followed them for years. Their work is changing how we think about our health and that diet and lifestyle can alter gene expression, and reverse and prevent chronic disease. For more on that, this post simply explains How Diet Pierces the Disease Epigenetics Process. The goal of Town Hall Medicine is to elevate the conversation on current health topics by providing information that is accurate, credible, proven and trusted.
Sign up for your two-week FREE access, hop around the different talks, and jump UP the microbiome learning curve to better health.
Here are just some of the talks you may find interesting…
- Stress and aging is talked about under “The New Path to Health”. Noodle around these recent studies in this area:
[Kimball et al 2017] found that in women, skin gene expression progressively changes from the 20s to the 70s in pathways related to oxidative stress, energy metabolism, senescence, and epidermal barrier and that these changes accelerated in the 60s and 70s. The gene expression patterns from the subset of women who were younger-appearing were similar to those in women who were actually younger! Here’s a good ScienceDaily article on this study, and this post simply explains How Diet Pierces the Disease Epigenetics Process. Suffice it to say, these skin epigenetic findings makes all the sense in the world — Eating a diet that supports your gut microbiota does GREAT things both inside our bodies and on the outside — I see these “side effect facelift” transformations everyday!
Concise Summary of SCD Studies
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
- Crohn’s Disease [Cohen et al. 2014; Suskind et al. 2014,Walters, et al.2014; Kakodkar et al. a 50 cohort, 2015; Suskind, et al, 2016] and
- UC [Obih et al. 2016; Suskind, et al, 2016].
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. 2014; Chassaing et al. 2015; Gewirtz et al. 2015; Nickerson 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. 2014; Suskind, 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-AID, University 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 a “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.”
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]:
- Half of a 417 patient survey use the SCD because of hesitation with medications used for IBD, and
- 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,
♥ 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.
Study Recruiting for Antibiotics, Autism Symptoms
Lots of children have autism.
Data from 2014, and confirmed in 2016, show 1 in 42 boys and 1 in 189 girls have autism. This is often put as one in 68 children have autism. The prevalence chart below shows the alarming autism increase since 2000. Also startling, the number of children with autism varies widely by community, from 1 in 175 children in areas of Alabama, to 1 in 45 children in areas of New Jersey. See CDC Autism State Report, 2014 and CNN Report, Autism rates now 1 in 68 U.S. children: CDC.
Autistic children’s microbiome metabolites (the exhaust of the gut microbiota) differs compared to children without autism.
Several studies have reported significantly higher oral antibiotic use in children with autism versus typical children (6, 14–17). Antibiotics cause collateral damage to the microbiome. From the 2016 review, The effects of antibiotics on the microbiome throughout development and alternative approaches for therapeutic modulation: The use of antibiotics heavily disrupts the ecology of the human microbiome (i.e., the collection of cells, genes, and metabolites from the bacteria, eukaryotes, and viruses that inhabit the human body). A dysbiotic microbiome may not perform vital functions such as nutrient supply, vitamin production, and protection from pathogens [3]. Dysbiosis of the microbiome has been associated with a large number of health problems and causally implicated in metabolic, immunological, and developmental disorders, as well as susceptibility to development of infectious diseases [4–11].
Why You Must Understand Epigenetics
Look… Your genes are not your destiny. Disease is rooted in our DNA EXPRESSION.
Epigenetics triggers disease in those predisposed.
Time to learn a short EASY bit more about epigenetics now that you know THIS is the real driver of your health status.
I love this video analogy of epigenetics: “What is Epigenetics? An Entertaining and Educational Primer”, GreenmedTV, April 2013. Look through the below slides to see how they use only PUNCTUATION VARIANCE TO DRAMATICALLY CHANGE UP THE DIALOGUE CONTEXT. This is a great analogy to what epigenetics does. EPIGENETICS DOES NOT “CHANGE UP” HUMAN DNA — that is constant for a lifetime. Rather, an EPIGENETIC CHANGE READS THE INFORMATION DIFFERENTLY AND EXPRESSES GENES ACCORDINGLY; THAT CAN BE BENEFICIAL OR DETRIMENTAL TO HEALTH AND DISEASE STATUS. I want you to think of this analogy as you read through the short EASY technicals of epigenetics because epigenetics is easier to get than it sounds! Here’s the bottom line: “Interactions with the environment do not change the genes, but they alter their expression by switching them on and off through chemical tags on the DNA“. — Gut microbes switch host genes on and off under influence of diet
Now for the technicals made EASY and simple: A module from Learning Genetics, from the University of Utah, called The Epigenome at a Glance explains:
- DNA contains the instructions for building all the parts of the body. DNA is wrapped around proteins called histones. Both the DNA and histones are covered with chemical tags. This second layer of structure is called the epigenome. See this in the below slide.
- The epigenome shapes the physical structure of the genome. It tightly wraps inactive genes making them unreadable. It relaxes active genes making them easily accessible. Different genes are active in different cell types. The human DNA code is fixed for life, but the epigenome is flexible.
- The epigenome changes in response to signals. Signals come from inside the cell, from neighboring cells, or from the outside world (environment). The signals from the outside world or environment that epigenetic tags react to include diet (things we eat are broken down and circulate throughout the body), stress (physical, emotional, chronic inflammation, disease), sleep, toxins, and more (see parameters on the below Whole Health Pillars slide). The epigenome adjusts specific genes in our genometic landscape in response to our rapidly changing environment.
- It is Proteins that Carry the Signals to the DNA. Once a signal reaches a cell, proteins carry information inside. Like runners in a relay race, proteins pass information to one another. The specifics of the proteins involved and how they work differ, depending on the signal and the cell type. But the basic idea is universal. The information is ultimately passed to a gene regulatory protein that attaches to a specific sequence of letters on the DNA.
- A gene regulatory protein attaches to a specific sequence of DNA on one or more genes. Once there, it acts like a switch, activating genes or shutting them down. Gene regulatory proteins also recruit enzymes that add or remove epigenetic tags. Enzymes add epigenetic tags to the DNA, the histones, or both. Epigenetic tags give the cell a way to “remember” long-term what its genes should be doing.
You can PLAY (so can your kidos!) with the epigenetic controls at this website to SEE and MAKE epigenetics happen! Just Do it… NOW!
The PEARL: Signals from the outside world can work through the epigenome to change a cell’s gene expression, moving towards health, or not.
Now for the University of Wisconsin-Madison diet study.
The study, Diet-Microbiota Interactions Mediate Global Epigenetic Programming in Multiple Host Tissues, with full text PDF here, found that gut microbes have a huge role in health as they alter the host gene expression in a diet dependent manner. The two diets studied, a plant based carbohydrate rich diet (think fruit/vegetables) compared to the Western, Standard American Diet (SAD) (think low fiber and high in simple carbs, sugars, and unhealthy fats found in most all home cooked/grocery prepared/restaurant foods as they use processed ingredients), expressed genes very differently not just in the gut, but in the liver and fatty tissue FAR removed from the gut. From the Wisconsin University News article, Gut’s microbial community shown to influence host gene expression:
Microbiome: Parkinson’s begins in the gut
The Study full text link is:
Gut Microbiota Regulate Motor Deficits and Neuroinflammation in a Model of Parkinson’s Disease, Dec 2016 and the PDF is here. The study looks at if changes in the immune response to gut bacteria could affect neurological outcomes, in particular motor symptoms in Parkinson’s. The study found that metabolites from the microbiome (this is the exhaust of the trillions of beasties) goes into circulation (it is not known yet if they make it into the brain) and these molecules impacted inflammation in the brain and motor symptoms.
Fasano, FREE: Early Nutrition Influences Microbiome, Disease
Your doc wasn’t taught this nor are they likely talking to you about microbiome and inflammation and how to move off the spectrum of inflammation, autoimmune and chronic disease. That is sad because many are learning about microbiome and changing diet and lifestyle to reduce that inflammatory microbiome disease tone. You can too by restoring and optimizing your microbiome. Contact me for the EASY How-To — that doesn’t break the bank either.
Listen in to Dr. Fasano, FREE, Early Nutrition Influences Microbiome, Disease!
REGISTER HERE, “How Early Nutrition Influences Gut Microbiome and Metabolic Profiles in Health and Disease: Shifting From a Disease-Centered Approach to Patient-Oriented Functional Medicine.”
Fiber Additives Starve Gut Microbes. They Eat Mucus Lining.
“While this work was in mice, the take-home message from this work for humans amplifies everything that doctors and nutritionists have been telling us for decades: Eat A LOT OF FIBER FROM DIVERSE NATURAL SOURCES,” says Martens. “Your diet directly influences your microbiota, and from there it may influence the status of your gut’s mucus layer and tendency toward disease. But it’s an open question of whether we can cure our cultural lack of fiber with something more purified and easy to ingest [fiber supplements or that added to processed foods] than a lot of broccoli.” —Eric Martens, Ph.D., an associate professor of microbiology at the University of Michigan Medical School who led the research along with his former postdoctoral fellow Mahesh Desai, Ph.D., now at the Luxembourg Institute of Health.
Move over gluten, ATI wrecks guts too.
Move over gluten, ATI wrecks guts too, and the damage goes beyond the gut!
This is cutting edge research, presented at the Opening Plenary Session at UEG Week Vienna 2016, which began October 15 and ran to Oct 19, 2016! You can listen live to these expert researchers, just sign into UEG. Obviously I have been! Regarding archiving content, I honestly don’t know UEG policy.
Proteins in wheat. There are a lot of different proteins in wheat and they are classified into groups, known as gliadins, glutenins, albumins and globulins.
Up to now, its been all about gluten (gliadin to be exact) and Celiac Disease and Non-Celiac Gluten Sensitivity (NCGS). Celiac has been well characterized over the last 4 decades. NCGS is the relative new comer. But with both conditions, what has not been known was what and how the innate immune system interacted. Researchers have been on the look out for the additional modulating factors, including cereal stimulants, of innate immunity, affecting signaling receptors for celiac disease, but until now, have not found the answer(s).
Now enters ANOTHER NEWLY FOUND WHEAT PROTEIN, a non-gluten wheat protein, called amylase-trpsin inhibitors (ATIs), that seems to be the what and how for activation of the innate system for wheat. ATIs are a subset of the albumin protein in wheat; ATIs are enriched in wheat and related cereals.
What does ATI innate immune activity do to the gut?
In sum, ATIs causes inflammation at the gut level that extends to inflammation beyond the gut including lymph nodes, spleen, kidney, and brain. When ATIs are fed to mice with autoimmunes or allergies, more severe disease and stronger antigen-specific adaptive immunity developed. Researchers agree that clinical studies are needed to determine whether this observation applies to humans with chronic inflammatory diseases. That would mean that consumption of wheat ATIs could worsen conditions such as RA, MS, IBD, asthma, lupus, alcoholic fatty liver disease, etc. ATIs also may contribute to the development of NCGS which includes association to IBS along with keen interest in associations to neurological conditions like autism, depression, AD, PD, etc.
The Studies.
From the 2015 Schuppan, et al paper,
Non-celiac wheat sensitivity: differential diagnosis, triggers and implications
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