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.
Multicenter, open label
This study included 12 patients ages 10 to 17 with mild or moderate Crohn’s disease (CD) or ulcerative colitis (UC). Nine children were from Seattle Children’s, and 3 were from Children’s Center for Digestive Health Care in Atlanta.
To determine if the specific carbohydrate diet (SCD) could have a positive impact on children with active inflammatory bowel disease (IBD)
The primary outcome measurement was the pediatric Crohn’s disease activity index (PCDAI) and pediatric ulcerative colitis activity index (PUCAI). Laboratory analysis of C-reactive protein (CRP) levels in the participants was also performed. Clinical follow-up took place at 2, 4, 8, and 12 weeks; each visit included a physical exam and blood CRP measurement in addition to completion of the PCDAI and PUCAI.
From a clinical perspective, I have found the SCD an indispensable tool in the management of patients with IBD.
Alterations in the patients’ fecal microbiome were also measured to gauge levels of dysbiosis. DNA extracted from stool in 9 of the 12 patients identified 201 bacterial species that either decreased or increased.
There were no adverse events reported; however, 2 patients dropped out of the study due to difficulty maintaining the diet. At the 2-week follow-up visit, 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 for 2 of the patients who maintained the diet for the full 12 weeks.
At 2 weeks, all but 1 patient had improvements or normalization of their CRP. The mean CRP remained below baseline levels at 8 weeks and 12 weeks.
Adherence to the diet for the 12-week period was correlated with significant changes in the microbial composition. Previous studies have shown that primary microbiota changes in patients with CD include a decrease in Firmicutes and Bacteroides commensal bacteria and an increase in proinflammatory bacteria such as Enterobacteriaceae.1,2 In this study, proteobacteria decreased in all of the patients except for one who had an unusually high proteobacteria level. There was an inverted abundance of Bacteroides and Firmicutes, from 67% and 31% (respectively) at baseline to 30% and 70% at 2 weeks. In this study, Bacteroides and Parabacteroides had the largest decrease in median abundance.
The SCD significantly restricts the intake of most carbohydrates. The diet became popular among children with IBD after the publication of the book Breaking the Vicious Cycle by Elaine Gottschall, whose 5-year-old daughter had ulcerative colitis.3 Hallmarks of the diet include:
- Use of nut flours such as almond and coconut to make breads and baked goods
- Added sugar limited to honey
- Dairy limited to fully fermented yogurt
- Avoidance of wheat, barley, corn, and rice
Because this diet is severely restrictive, compliance is an issue. In addition, it is unknown why some patients have positive outcomes and others do not.
Results from this study are consistent with previously published reports including a 2016 study published in Nutrition by Obih et al.4,5 In the Obih retrospective review, PCDAI and PUCAI significantly improved for the majority of the children in the study.6
From a clinical perspective, I have found the SCD an indispensable tool in the management of patients with IBD. It doesn’t always work to produce remissions as a standalone intervention, but at the very least it seldom fails to ameliorate symptoms. Responses vary from patient to patient and depend on long-term adherence, which is challenging.
Further supporting the efficacy of the diet is my frequent clinical observation that patients who initially succeed with the SCD tend to experience disease flares if they lapse in their compliance.
The rationale for the diet is to alter the microbiome by breaking the cycle of proliferation of pathogenic intestinal bacteria. Current theories about the causation of IBD highlight the role of the microbiota in triggering the cytokine cascade that leads to barrier disruption and inflammation. Changing the nutritional substrate for microbial growth may suppress harmful species and allow the re-emergence of a healthy microbiome conducive to healing.
The SCD bears some similarities to 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 Gut and Psychology Syndrome (GAPS) diets, which are also thought to influence gut ecology.
I learned of the SCD in the early 1990s through the work of Elaine Gottschall, who first published Food and Gut Reaction in 1987, subsequently renamed Breaking the Vicious Cycle. The book has sold well over a million copies, and I was invited to write the introduction for a subsequent edition.
Gottschall first encountered the diet while seeking an alternative to colectomy for her 8-year-old daughter, who suffered from ulcerative colitis. Her daughter had also been diagnosed with “infantile schizophrenia,” a now-discarded term for what was likely an autism spectrum disorder.
After consulting numerous specialists who offered her little hope beyond radical surgery, she sought help from a 92-year-old German-trained physician, Dr. Sidney Valentine Haas. In 1951, Dr. Haas proposed a prototype of the SCD in his book Management of Celiac Disease.7
Gottschall implemented the Haas diet, and her daughter’s gastrointestinal (GI) symptoms abated, ultimately achieving full remission. More remarkably, her neurodevelopmental problems receded. Gottschall was so impressed that she obtained degrees in nutritional biochemistry and cellular biology to better understand and communicate the benefits of the SCD.8 She became a tireless and outspoken proponent of the diet until her death in 2005. In this way, she anticipated by several decades our present understanding of the role of dysbiosis as a driver of GI pathology.
Nevertheless, in 2012, the Crohn’s and Colitis Foundation (CCFA) issued this official position about the SCD: “There is no evidence to suggest 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 trials, evidence substantiating the benefits of the SCD is becoming incontrovertible. Surveys of adherents to the diet consistently document improvements.10 Mostly due to activism from the SCD community, the CCFA recently accepted an award of $2.5 million from the Patient-Centered Outcomes Research Institute (PCORI) to study the effectiveness of the specific carbohydrate diet vs the Mediterranean-style diet for inducing remission in patients with Crohn’s disease.11
In my experience, the challenge to the clinician lies in properly adjusting the parameters of the SCD to target the patient’s individual circumstances. While I often use it as a starting point, the SCD may require modification.
For example, while the SCD permits dairy in the form of homemade yogurt (because fermentation greatly reduces lactose content), some patients are intolerant not to the lactose content of milk, but to casein or lactalbumin. Other patients may have trouble with the preponderance of nut flours that are baking substitutes in the SCD.
Additionally, introduction of SCD foods must be carefully staged, especially in patients with acute flares or strictures. Some may only tolerate a low-residue version of the SCD for a while, consisting mostly of broths and well-cooked animal protein, with avoidance of raw fruits and vegetables. Caloric support may be achieved with coconut oil or medium-chain triglyceride (MCT) oil.
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, with consequent mucosal ulceration.12 The major dietary sources of sulfur include red meat, fish, nuts, eggs, and Brassica vegetables, which are included in the SCD. For some patients, a trial of reduction of high-sulfur foods might prove warranted if they are not responding to the SCD.
One way to attenuate the effects of hydrogen sulfide, as well as support the metabolism of colonic mucosa, is via provision of short-chain amino acids, especially butyrate. The best way to boost intestinal butyrate is by consumption of fiber that provides intestinal microbes with a fermentable substrate for synthesis of short-chain fatty acid metabolites. But these are the very “resistant starches” that are prohibited on the SCD.
Hence “Gibson’s Conundrum,” proposed by Peter Gibson, a researcher at Monash University in Australia, whose department of gastroenterology is known for research on the low-FODMAP diet. Gibson notes that there may be 2 competing rationales for diet modification in IBD: a low-FODMAP diet like the SCD that attenuates symptoms, and a high–resistant starch diet that fosters production of short-chain fatty acids. He writes:
The conclusion reached is that, while both approaches may alleviate symptoms in both IBS [irritable bowel syndrome] and IBD, there is insufficient data yet to determine whether both approaches lead to equivalent bacterial effects in mollifying the immune system. This is particularly relevant in IBD. As such, caution is urged to use long-term carbohydrate withdrawal in IBD in remission to control IBS-like symptoms.13
One possible solution is to add resistant starch to the SCD. The efficacy of resistant starch for IBD has been supported in some studies.14 I usually consider this option after an acute flare resolves and the patient is showing signs of improvement with reduced 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 then cooled potatoes or parboiled rice; green bananas; plantains; or unmodified potato starch (none of which are acceptable on the SCD). Addition of these foods provides variety and alternative calorie sources, and may help sustain remission in SCD responders.
An obstacle to recovery with the SCD may be the inadvertent inclusion of microparticles (titanium dioxide and aluminosilicates), emulsifiers (eg, polysorbate 80 and carboxymethylcellulose), and carrageenan, which are not strictly addressed by Gottschall. These substances, while generally recognized as safe and therefore frequently included in processed foods and even supplements, have been shown to have deleterious effects on the gut epithelial layer.15-18
It's worth mentioning that the SCD can be valuable in the management of other conditions, such as diverticulitis. It also helps “stuck” patients with documented celiac disease whose symptoms fail to resolve completely with just gluten elimination (“nonresponsive celiac disease”). Lastly, a sizeable number of parents of kids with autistic spectrum disorders are carefully implementing the SCD to address the dysbiosis that is thought to be a component of that condition.19
- Fujimoto T, Imaeda H, Takahashi K, et al. Decreased abundance of Faecalibacterium prausnitzii in the gut microbiota of Crohn’s disease. J Gastroenterol Hepatol. 2013;28(4):613-619.
- Frank DN St, Amand AL, Feldman RA, et al. Molecularphylogenetic characterization of microbial community imbalances in human inflammatory bowel diseases. Proc Natl Acad Sci U S A. 2007;104(34):13780-13785.
- Gottschall E. Breaking the Vicious Cycle: Intestinal Health Through Diet. Baltimore, Ontario: Kirkton Press; 1994.
- Suskind DL, Wahbeh G, Gregory N, Vendettuoli H, Christie D. Nutritional therapy in pediatric Crohn disease: the specific carbohydrate diet. J Pediatr Gastroenterol Nutr. 2014;58(1):87-91.
- Cohen SA, Gold BD, Oliva S, et al. Clinical and mucosal improvement with specific carbohydrate diet in pediatric Crohn disease. J Pediatr Gastroenterol Nutr. 2014;59(4):516-521.
- Obih C, Wahbeh G, Lee D, et al. Specific carbohydrate diet for pediatric inflammatory bowel disease in clinical practice within an academic IBD center. Nutrition. 2016;32(4):418-425.
- Haas SV, Haas MP. Management of Celiac Disease. Philadelphia, PA: JB Lippincott; 1951.
- Breaking the Vicious Cycle: Intestinal Heath Through Diet with the Specific Carbohydrate Diet website: http://www.breakingtheviciouscycle.info/p/about-the-author/. Accessed February 28, 2017.
- The Specific Carbohydrate Diet (SCD). Crohn’s and Colitis Foundation website: http://www.crohnscolitisfoundation.org/resources/specific-carbohydrate-diet.html. Published June 1, 2012. Accessed February 28, 2017.
- SCD Survey Update. SCD Research web site: http://www.scdresearch.com/scd-survey-results.html. Updated June 18, 2015. Accessed February 28, 2017.
- First-Ever National Study of Dietary Interventions to Treat Crohn’s Disease Receives Funding. Crohn’s and Colitis Foundation web site: http://www.ccfa.org/news/dietstudy.html. Published March 24, 2016. Accessed February 28, 2017.
- Jowett SL, Seal CJ, Pearce MS, et al. Influence of dietary factors on the clinical course of ulcerative colitis: a prospective cohort study. Gut. 2004;53(10):1479-1484.
- Fung QM, Szilagyi A. Carbohydrate elimination or adaptation diet for symptoms of intestinal discomfort in IBD: rationales for "Gibsons' Conundrum". Int J Inflam. 2012;2012:493717.
- Jacobasch G, Schmiedl D, Kruschewski M, Schmehl K. Dietary resistant starch and chronic inflammatory bowel diseases. Int J Colorectal Dis. 1999;14(4-5):201-211.
- Pietroiusti A, Magrini A, Campagnolo L. New frontiers in nanotoxicology: gut microbiota/microbiome-mediated effects of engineered nanomaterials. Toxicol Appl Pharmacol. 2016;299:90-95.
- Powell JJ, Ainley CC, Harvey RS, et al. Characterisation of inorganic microparticles in pigment cells of human gut associated lymphoid tissue. Gut. 1996;38(3):390-395.
- Viennois E, Merlin D, Gewirtz AT, Chassaing B. Dietary emulsifier-induced low-grade inflammation promotes colon carcinogenesis. Cancer Res. 2017;77(1):27-40.
- Borthakur A, Bhattacharyya S, Anbazhagan AN, Kumar A, Dudeja PK, Tobacman JK. Prolongation of carrageenan-induced inflammation in human colonic epithelial cells by activation of an NFκB-BCL10 loop. Biochim Biophys Acta. 2012;1822(8):1300-1307.
- Vuong HE, Hsiao EY. Emerging roles for the gut microbiome in autism spectrum disorder. Biol Psychiatry. 2017;81(5):411-423.