Study: The specific carbohydrate diet for chronic inflammatory bowel disease

Relation

Suskind DL, Cohen SA, Brittnacher MJ, et al. Clinical and fecal microbial changes with diet therapy in active inflammatory bowel disease [published online ahead of print December 27, 2016].J Clin Gastroenterol.

Draft

Multicenter, open label

Participant

This study included 12 patients aged 10 to 17 years with mild or moderate Crohn's disease (CD) or ulcerative colitis (UC). Nine children came from Seattle Children’s and 3 from the Children’s Center for Digestive Health Care in Atlanta.

Study objective

To determine whether the specific carbohydrate diet (SCD) could have a positive impact on children with active inflammatory bowel disease (IBD).

Target parameters

The primary outcome measure was the pediatric Crohn's disease activity index (PCDAI) and the pediatric ulcerative colitis activity index (PUCAI). Laboratory analysis of C-reactive protein (CRP) levels in participants was also performed. Clinical follow-up examinations took place at 2, 4, 8 and 12 weeks; Each visit included a physical examination and blood CRP measurement in addition to performing PCDAI and PUCAI.

From a clinical perspective, I have found the SCD to be an essential tool in the treatment of patients with IBD.

Changes in the patients' fecal microbiome were also measured to estimate the extent of dysbiosis. DNA extracted from the stool of 9 of the 12 patients identified 201 species of bacteria that either decreased or increased.

Key insights

No adverse events were reported; however, 2 patients discontinued the study due to difficulty adhering to the diet. At the 2-week follow-up, 5 of the 12 patients were in clinical remission. Eight of the remaining 11 patients achieved remission at 8 weeks, and 8 of 10 remained in remission at 12 weeks. Therapy was ineffective in 2 of the patients who remained on the diet for the entire 12 weeks.

After 2 weeks, all but 1 patient had improvement or normalization of their CRP. Mean CRP remained below baseline values ​​at 8 weeks and 12 weeks.

Diet adherence over the 12-week period was correlated with significant changes in microbial composition. Previous studies have shown that the changes in the primary microbiota in patients with celiac disease include a decrease inFirmicutesandBacteroidscommensal bacteria and an increase in proinflammatory bacteria such as:Enterobacteria.^1.2In this study, Proteobacteria decreased in all patients except one who had an unusually high level of Proteobacteria. There was a reverse abundance ofBacteroidsandFirmicutes, from 67% and 31% at baseline to 30% and 70% at 2 weeks. In this study,BacteroidsandParabacteroideshad the largest decrease in mean frequency.

Practice implications

SCD significantly limits the intake of most carbohydrates. The diet became popular among children with IBD after the book was publishedBreak the vicious circleby Elaine Gottschall, whose 5-year-old daughter suffered from ulcerative colitis.³Characteristics of the diet are:

• Verwendung von Nussmehlen wie Mandel- und Kokosmehl zur Herstellung von Brot und Backwaren
• Zuckerzusatz beschränkt auf Honig
• Milchprodukte sind auf vollständig fermentierten Joghurt beschränkt
• Vermeidung von Weizen, Gerste, Mais und Reis

Because this diet is highly restrictive, adherence is an issue. Furthermore, it is unknown why some patients have positive results and others do not.

The results of this study are consistent with previously published reports, including a 2016 study published inNutritionby Obih et al.^4.5In Obih's retrospective review, PCDAI and PUCAI improved significantly in the majority of children in the study.⁶

From a clinical perspective, I have found the SCD to be an essential tool in the treatment of patients with IBD. Producing remissions as a standalone intervention does not always work, but at least it rarely fails to relieve symptoms. Responses vary from patient to patient and depend on long-term adherence, which is challenging.

Further supporting the diet's effectiveness is my frequent clinical observation that patients who are initially successful with SCD tend to experience disease flares as they lose compliance.

The rationale for the diet is to change the microbiome by breaking the cycle of proliferation of pathogenic intestinal bacteria. Current theories about the causes of IBD highlight the role of the microbiota in triggering the cytokine cascade that leads to barrier dysfunction and inflammation. Changing the nutrient substrate for microbial growth can suppress harmful species and allow the reemergence of a healthy microbiome that is conducive to healing.

The SCD shares some similarities with the Paleo, low-FODMAP (FODMAP stands for fermentable oligosaccharides, disaccharides, monosaccharides and polyols, short-chain carbohydrates that are incompletely absorbed from the gastrointestinal tract), and the Gut and Psychology Syndrome (GAPS) diet. which are also thought to influence gut ecology.

I learned about the SCD in the early 1990s through the work of Elaine Gottschall, who first published itFood and intestinal reaction1987, later renamedBreak the vicious circle. The book has sold well over a million copies, and I was invited to write the introduction to a subsequent edition.

Gottschall first came across the diet when she was looking for an alternative to colectomy for her 8-year-old daughter, who had ulcerative colitis. Her daughter had also been diagnosed with “infantile schizophrenia,” a now-defunct term for a probable autism spectrum disorder.

After consulting numerous specialists who gave her little hope beyond radical surgery, she sought help from a 92-year-old German-trained doctor, Dr. Sidney Valentine Haas. In 1951 Dr. Haas presents a prototype of the SCD in his bookTreatment of celiac disease.⁷

Gottschall introduced the Haas diet, and her daughter's gastrointestinal (GI) symptoms subsided, eventually achieving complete remission. Even more remarkable is that her neurodevelopmental problems regressed. Gottschall was so impressed that she pursued degrees in nutritional biochemistry and cell biology to better understand and communicate the benefits of SCD.⁸She became a tireless and outspoken advocate of the diet until her death in 2005. In doing so, she anticipated our current understanding of the role of dysbiosis as a driving force of GI pathology by several decades.

Nevertheless, in 2012, the Crohn's and Colitis Foundation (CCFA) published this official position on SCD: "There is no evidence that any particular food or diet causes, prevents, or cures inflammatory bowel disease."⁹

But with the advent of this recent study and other previous small studies, the evidence supporting the benefits of SCD is becoming irrefutable. Surveys of dieters consistently document improvements.¹⁰Largely due to the activism of the SCD community, the CCFA recently accepted a $2.5 million award from the Patient-Centered Outcomes Research Institute (PCORI) to study the effectiveness of the specific carbohydrate diet compared to the Mediterranean diet for inducing remission in patients with Crohn's disease.¹¹

In my experience, the challenge for the clinician is to properly adjust the parameters of the SCD to take into account the patient's individual circumstances. Although I often use it as a starting point, the SCD may need to be modified.

For example, while SCD allows dairy products in the form of homemade yogurt (because fermentation greatly reduces the lactose content), some patients cannot tolerate the lactose content of milk but can tolerate casein or lactalbumin. Other patients may have problems with the predominance of nut flours, which are baking substitutes, in the SCD.

Furthermore, the introduction of SCD foods must be carefully staggered, particularly in patients with acute flares or strictures. Some may only tolerate a low-residue version of the SCD, consisting primarily of broths and well-cooked animal proteins, avoiding raw fruits and vegetables. Calorie support can be achieved with coconut oil or medium chain triglyceride oil (MCT).

Finally, some theorize that hydrogen sulfide may contribute to the pathogenesis of ulcerative colitis. High concentrations have been shown to increase intestinal permeability and alter barrier function, leading to mucosal ulcers.¹²The main dietary sources of sulfur include red meat, fish, nuts, eggs and brassica vegetables, which are found in the SCD. In some patients, an attempt to reduce sulfur-rich foods may be warranted if they do not respond to SCD.

One way to weaken the effects of hydrogen sulfide and support the metabolism of the colon mucosa is to provide short-chain amino acids, especially butyrate. The best way to increase intestinal butyrate is to consume fiber, which provides intestinal microbes with a fermentable substrate for the synthesis of short-chain fatty acid metabolites. But these are the very “resistant starches” that are banned on the SCD.

Hence “Gibson’s Conundrum,” suggested by Peter Gibson, a researcher at Monash University in Australia whose department of gastroenterology is known for researching the low-FODMAP diet. Gibson notes that there may be two competing reasons for dietary change in IBD: a low-FODMAP diet like the SCD, which lessens symptoms, and a high-resistant starch diet, which promotes the production of short-chain fatty acids. He writes:

The conclusion is that while both approaches may relieve symptoms in both IBS [irritable bowel syndrome] and IBD, there is not yet enough data to determine whether both approaches result in equivalent bacterial effects in calming the immune system. This is particularly relevant in IBD. Therefore, caution is advised to use long-term carbohydrate deprivation for IBD in remission to control IBS-like symptoms.¹³

A possible solution is to add resistant starch to the SCD. The effectiveness of resistant starch for IBD has been proven in some studies.¹⁴I usually consider this option after an acute episode has resolved and the patient shows signs of improvement with decreased stool frequency and/or abdominal pain after a few weeks or months of adherence to the SCD. Well-tolerated sources of resistant starch include cooked and then cooled potatoes or parboiled rice; green bananas; plantains; or unmodified potato starch (neither of which is acceptable on the SCD). The addition of these foods provides variety and alternative sources of calories and may help maintain remission in SCD responders.

An obstacle to recovery with the SCD can be the accidental inclusion of microparticles (titanium dioxide and aluminosilicates), emulsifiers (e.g., polysorbate 80 and carboxymethylcellulose), and carrageenan, which are not specifically addressed by Gottschall. Although these substances are generally recognized as safe and are therefore often found in processed foods and even dietary supplements, they have been shown to have harmful effects on the intestinal epithelial layer.^15-18

It is worth noting that SCD can be used in the treatment of other diseases such as: B. diverticulitis, can be valuable. It also helps “stuck” patients with documented celiac disease whose symptoms do not fully resolve with elimination of gluten (“unresponsive celiac disease”). Finally, a significant number of parents of children with autism spectrum disorders carefully use SCD to address the dysbiosis that is believed to be a component of this disorder.¹⁹