The Specific Carbohydrate Diet
To better understand how the Specific Carbohydrate Diet™ (SCD™) may work, it is helpful to first examine current theories on what might cause IBD.
To date, IBD is still considered an idiopathic disease. This means that there is no clinically proven, medically accepted cause for the disease. However, there are numerous theories on factors that may lead to, exacerbate, or accelerate IBD.
Researchers have theorized that IBD may result from a combination of factors, including an abnormal response by the body’s immune system to intestinal bacteria, an overabundance of bacteria in the digestive tract, genetic predisposition, and various environmental factors.[1,2,3,4,5]
In regard to genetic factors, multiple studies have suggested that first-degree relatives of individuals with IBD may have a 4 to 20 times higher risk of developing the disease themselves compared to the general population, and the risk of developing the disease if a family member already has it is approximately 7%.[6,7] While the underlying reasons for this are still unknown, researchers have already uncovered a number of genomic linkages to IBD, including mutations of the NOD2-encoding gene in certain Crohn’s patients. Theories about an environmental connection to IBD have arisen from the fact that the prevalence of the disease in certain regions of the world has paralleled the adoption of a lifestyle that includes a Western diet, smoking, oral contraceptive use, and greater levels of stress.
Research into the genetic and environmental factors that influence IBD is critical. With a better understanding of causal factors for the disease, we may one day be able to prevent the onset of IBD or more effectively treat the underlying conditions. However, the research that is most relevant for understanding how the SCD™ purports to work involves how the immune system functions in relation to bacterial populations in the digestive tract of individuals with IBD.
Very recent studies into the immune function of individuals with IBD reveal an imbalance of regulatory cells and attack cells in the blood and intestinal mucosa. Relative to the general population, IBD patients exhibit fewer regulatory T Cells and more Th17 “attacker” cells. This imbalance leads to an abnormal immune response in which the body attacks microbes resident in the intestinal tract, leading to inflammation.
In addition to this altered immune function, there is considerable evidence that bacteria play a central role in the onset and perpetuation of IBD.[4,11,12,13] Studies of the bacterial population in patients with IBD reveal a decrease in the number of beneficial bacteria (including Lactobacillus) and an increase in the number of pathogenic, malignant bacteria such as Bacteroides and E. coli. This breakdown in the balance of protective versus harmful bacteria may further promote inflammation.[14,15,16]
As a result of some of these findings, an increasing number of doctors and researchers now suspect that the combination of an overly aggressive inflammatory response coupled with an overpopulation of harmful bacteria in the intestinal tract plays a central role in the perpetuation of the disease. Exactly what this role is, and how it may relate to the onset and persistence of IBD, is the subject of ongoing clinical study.
Elaine Gottschall, who researched and popularized the SCD™, has theorized that in the digestive tract of the individual with IBD there exists a microbial imbalance. Specifically, she has suggested that these patients possess an overgrowth of bacteria in the stomach and small intestine, which leads to an increase in harmful waste products which these microbes release.
The byproducts of this microbial overgrowth may include the production of excess short chain organic acids and an increase in bacterial toxins. These acids and toxins have the potential to severely damage digestive enzymes on the intestinal cell surface, which in turn leads to (1) the triggering of an inflammatory response as the body attempts to fight off the perceived bacterial threat, (2) the production of excessive mucus as the intestinal tract attempts to lubricate itself against the irritation caused by the toxins and acids, and (3) difficulty digesting and absorbing certain carbohydrates.
Researchers have found that damage to the enzyme-containing microvilli on the intestinal surface can prevent the complete digestion of many carbohydrates, leading to an accumulation of undigested carbohydrates in the small intestine.[18,19,20,21] Of the various energy sources available, undigested carbohydrates have been shown to have the greatest impact on intestinal microbial growth. These undigested sugars that remain in the intestinal lumen serve as the fuel bacteria need to multiply.[23,24]
As these microbes and bacteria multiply in the intestinal tract, Ms. Gottschall has proposed that their byproducts increase accordingly. This would create a destructive cycle in which the microbial toxins and acid byproducts damage the digestive enzymes, leading to systematic malabsorption of the very carbohydrates that fuel the continued bacterial growth. The mucus produced as a defense mechanism by the intestinal cells may, in fact, aggravate the malabsorption by blocking contact between the digestive microvilli enzymes and the disaccharides lactose, maltose, sucrose, and isomaltose, as well as starch molecules (polysaccharides). This, in essence, is the ―vicious cycle‖ Ms. Gottschall refers to in her book.
The SCD™ aims to disrupt this cycle by manipulating the energy supply of the intestinal microbes. The diet severely limits the availability of carbohydrates as a food source, which gradually reduces the number of bacteria and the quantity of their waste and toxins. As conditions in the small intestine improve, malabsorption is eventually replaced by absorption, and the cells of the body are once again properly nourished. The volume of sugar fermenting in the digestive tract then declines, which may reduce the physical symptoms of pain, gas, and diarrhea.
The diet achieves these benefits by dramatically restricting the consumption of disaccharides and polysaccharides, which require splitting by intestinal enzymes before they are absorbed into the body. The diet promotes the consumption of primarily monosaccharide carbohydrates (carbohydrates that are single sugars, such as glucose, fructose, and galactose), which generally require no further splitting in order to be absorbed into the bloodstream. By limiting the patient to “predigested” carbohydrates, the bacteria are gradually reduced due to lack of available food, and normal digestion can be restored.  The patient is also allowed to eat eggs, meats, and certain fats, in addition to single-sugar carbohydrates, such as those contained in most fruits and vegetables.
The obvious question, of course, is does the SCD™ really work? Our take on the evidence is that it appears to be effective in helping patients with IBD, although there is a clear need for more research in this area. What we do know is that thousands and thousands of people appear to have used the diet successfully to treat the disease. Their stories are very well documented on numerous websites, in the form of attributed testimonials and survey responses. However, relatively few clinical studies have specifically examined the efficacy of the SCD™, which highlights the difficulty researchers have obtaining funding when a medication is not the subject of inquiry. The studies that have been done, while small in scope, seem to suggest that the diet holds great promise for individuals suffering from IBD.
One study, conducted by Leo Galland, MD, was published in the journal Alternative Therapies and looked at healing rates among a population of 20 Crohn’s patients. The diet’s rate of effectiveness in bringing about remission or near remission of symptoms was stated to be 55%. While these results are encouraging, it is possible that the actual success rate for people with Crohn’s is even higher. Dr. Galland gave patients one month to respond to the diet, and in the event that a 50% reduction in symptoms was not achieved within that time period, non-glutenous starch (such as rice and potatoes) was reintroduced to the diet. The SCD™ specifically strictly forbids the consumption of these starches. Still, the 55% success rate should be viewed favorably in light of the relatively short period of study.
In 2004, a case study on the SCD™ was published in Tennessee Medicine. The report highlighted two patients, a woman with ulcerative colitis and a man suffering from Crohn’s disease. Both had significant complications arising from their respective diseases that were completely resolved through following the SCD™. At the time, the lead author, Raquel Nieves, MD, called for more research into the diet as a primary tool to treat IBD.
In 2011, Professor Barbara Olendzki at the University of Massachusetts Medical Center released an abstract of a study on a diet similar to the SCD. The Anti-Inflammatory Diet for IBD (IBD-AID) was derived from the SCD, with slight modifications. For example, the IBD-AID restricted the consumption of certain trans-fatty acids, and added probiotics to the diet regimen. In the study, 100% of the 11 subjects showed dramatic improvement in disease markers (measures of disease activity) over a 6-10 month period, and 9 of 11 subjects were able to reduce or eliminate their use of medication to treat their IBD.
While these initial findings are encouraging, it is unfortunate that more researchers have not investigated the SCD™ as a first line treatment for IBD. As a means of addressing the gap in SCD-specific research, proponents of the diet often point to studies on the Elemental Diet as validation of the science underlying Ms. Gottschall’s approach. In a number of ways, the SCD™ is similar to the synthetic Elemental Diet, which has been studied extensively in the treatment of digestive disorders.
Unlike the SCD™, the Elemental Diet is frequently administered in a hospital via a feeding tube and the chemical nutrients have been assembled in a laboratory. Therefore, any improvement in health is often temporary and is reversed when the patient leaves the facility and returns to a standard diet. Much like the SCD™, the type of carbohydrate which predominates in elemental diets is the single sugar monosaccharide, glucose, which is readily absorbed by the body. For this reason, Ms. Gottschall has argued that the chemical similarity between the two diets means that research on the effectiveness of elemental diets in the hospital provides support for the use of the SCD™ in the home.
The safety and efficacy of the Elemental Diet (and its variants) is well established in medical literature, and various studies have demonstrated its effectiveness in correcting malabsorption and improving many intestinal disorders.[29,30] In certain Asian countries, including Japan, elemental diet therapies are still the preferred primary remission-induction tool for active intestinal inflammation, rather than corticosteroid therapy. However, in Western countries such as the U.S., elemental diets have been largely neglected in favor of corticosteroid therapy.
Explaining the various reasons why Western Medicine has failed to embrace diet as a primary tool to treat IBD is complicated. However, variability in the research data has clearly played a role. For example, in 1990 a large scale study of 113 patients with Crohn’s was published in the journal Gut. The study was retrospective and covered ten years, with patient outcomes tracked over five years. An elemental diet was successful in achieving remission in 96 of the 113 Crohn’s patients (85%), with relatively low relapse rates. This remission rate compared favorably to that achieved with steroids.  However, the very next year, the European Cooperative Crohn’s Disease Study was published, which reported very different remission rates. This study, which examined 107 adults with moderate to severe Crohn’s, found that 53% of patients on an elemental diet achieved remission, compared to 85% on a steroid regimen. 
Overall, studies on elemental diets have demonstrated considerable variability. Some have shown that these diets have remission rates on par or even better than steroids, while others have strongly suggested the superiority of drug therapies. Such differences could be the result of the therapeutic duration of the diet, the composition of elemental diets used, and also the criteria for remission. It is worth noting that some of the recent studies that have demonstrated impressive remission rates using elemental diets have included specific additives to their dietary formulas, including omega 3 fatty acids, transforming growth factors that combat inflammation, and probiotics.
Regardless of the source of variation in the studies, Western Medicine has continued to favor the use of steroid therapy, due in part to the perception that elemental diets are difficult to administer (they may require a hospital stay) and patient compliance with medication will be higher. The SCD™ attempts to overcome these issues by approximating the chemical composition of the elemental diet, but in a form that can be administered over the long-term and allows for a more varied menu of food options. Additionally, the use of diet to treat IBD overcomes two major shortcomings of traditional corticosteroid therapy, being (1) the adverse side effects, and (2) the lack of a demonstrated healing effect from use.
A widely acknowledged problem with conventional drug therapy is the frequency and severity of adverse side effects and the toxicity of these medications when they are administered over the long term. [35,36] In the case of corticosteroids, side effects may include sleep disturbances, mood changes, fatigue, headaches, upset stomach, and the potential for hypertension, hyperglycemia, thinning of the skin, seizures, and other adverse conditions. [37,38] Side effects for 5-ASA drugs include nausea or upset stomach, muscle and joint aches and pains, and headaches. Less frequently, this therapy causes inflammation of the liver, acute inflammation of the pancreas, inflammation of the lungs, low red blood cell count, and suppression of blood cell formation in bone marrow.  We believe it is important to weigh the potential for side effects in making a decision to treat IBD with a particular therapy. One significant benefit of the SCD™ is the apparent lack of adverse side effects.
It is important also to consider the healing effects of diet when compared to drug therapy. Studies have shown that elemental diet therapy induces radiographic and endoscopic remission, meaning that healing of the intestinal surface or colon is present. In contrast, there have been limited cases where drug therapies showed meaningful improvement in radiographic and endoscopic findings. Additional research has suggested that healing of the intestinal mucosa is significantly higher in patients using enteral nutrition therapy as opposed to a steroid protocol. 
The apparent discrepancy in rates of healing between treatment modalities is supported by a 2004 study by Kobayashi and his colleagues that compared home enteral nutrition (essentially a liquid version of an elemental diet that can be taken at home) with drug therapy for the treatment of Crohn’s patients. These researchers conducted a long-term comparison of complications and surgery rates between dietary treatment and drug therapy, and found that both were higher in the drug therapy group. The researchers noted that continuous enteral nutrition was a useful approach to “prevent progression to intestinal complications and also to avoid surgical operations.”  Ms. Gottschall has suggested the SCD™ is a practical way to get the benefits of an entural diet without sacrificing food variety, which might lead to higher patient compliance. 
We recognize that you just read through quite a bit of science in a short period of time. The amazing thing is that was only a small sampling of the research currently being conducted on IBD. All of us should take solace in the fact that some very smart minds are at this very moment researching what could turn out to be the next big breakthrough in IBD treatment. We hope it comes soon.
So, a logical question is “where does all this research and data leave us?” In summarizing the direct support for the SCD™, one could reasonably state that the anecdotal evidence is very strong, while significantly more work needs to be completed on the clinical research side to validate the diet’s effectiveness across a broad patient population.
Still, we feel that there is sufficient reason to recommend the diet to patients with Crohn’s and ulcerative colitis. The SCD™ in many ways approximates the approach of elemental diets, but makes it practicable for patients to follow the therapy in their daily life. Therefore, the SCD™ eliminates one of the primary objections to the use of the elemental diet as a long-term solution for IBD, being that the improvements may reverse once the patient leaves the hospital and goes off the diet. Additionally, we like the fact that the SCD™ may limit the patient’s exposure to adverse drug side effects in the event that medication can be gradually reduced if the diet is successful in inducing remission.
Food Rx will continue to look for ways to sponsor and support more research into the effectiveness of the SCD™ in the clinical setting. In the meantime, we are encouraged by anecdotal reports that suggest long-term remission is possible when following the diet, and that should be welcome news to patients.
Next Section: How to Follow the Diet
 Su C, Lichtenstein. Ulcerative colitis. In M Feldman et al., eds., Sleisenger and Fordtran’s Gastrointestinal and Liver Disease, 2008; 8th ed., vol. 2, pp. 2499-2548.
 Bradesi, S, etl al. Inflammatory bowel sisease and irritable bowel syndrome: altered immune system and inflammation in inflammatory bowel diseases. Curr Opin Gastroenterol. 2003;19(4).
 Barnich, N, et al. Role of bacteria in the etiopathogenesis of inflammatory bowel disease. World J Gastroenterol 2007; 13(42): 5571-5576.
 Podolsky DK. Inflammatory bowel disease. N Engl J Med. 2002; 347: 417-429.
 Lakatos, P. Environmental factors affecting inflammatory bowel disease: have we made progress? Dig Dis 2009;27:215-225.
 Tysk C, et al. Ulcerative colitis and Crohn’s disease in an unselected population of monozygotic and dizygotic twins: a study of heritability and the influence of smoking. Gut 1988; 29:990-6.
 Orholm M, et al. Familial occurrence of inflammatory bowel disease. N Engl J Med 1991;324:84-8.
 Ogura Y, et al. A frameshift mutation in NOD2 associated with susceptibility to Crohn’s disease. Nature 2001;411: 603-6.
 Yamamoto T, et al. Diet and inflammatory bowel disease – epidemiology and treatment. Alimentary Pharmacology & Therapeutics. 2009;30(2):99-112.
 Eastaff-Leung N, et al. Foxp3+ regulatory T Cells, Th17 Effector Cells, and Cytokine environment in inflammatory bowel disease. J Clin Immunol. 2010; 30(1):80-9.
 Sartor RB. Intestinal microfl ora in human and experimental inflammatory bowel disease. Curr Opin Gastroenterol. 2001; 17:324-330.
 Farrell R, et al. Microbial factors in inflammatory bowel disease. Gastroenterol Clin North Am. 2002; 31: 41-62.
 Shanahan F. Host-flora interactions in inflammatory bowel disease. Infl amm Bowel Dis. 2004; 10 Suppl 1: S16-S24.
 Swidsinski A, et al. Mucosal flora in inflammatory bowel disease. Gastroenterology 2002; 122: 44-54.
 Neut C, et al. Changes in the bacterial fl ora of the neoterminal ileum after ileocolonic resection for Crohn’s disease. Am J Gastroenterol 2002; 97: 939-946.
 Darfeuille-Michaud A, et al. Presence of adherent Escherichia coli strains in ileal mucosa of patients with Crohn’s disease. Gastroenterology 1998; 115: 1405-1413.
 Gottschall E. Digestion-gut-autism connection: the Specific Carbohydrate Diet. Medical Veritas. 2004; 1:261-271
 Moog F. The lining of the small intestine. Scientific American, 1981; 245:154–76.
 Prinsloo JG, et al. Lactose absorption and mucosal disaccharidases in convalescent pellagra and kwashiorkor children. Archives of Diseases of Childhood. 1971;46:474–8.
 Campos J, et al. Jejunal mucosa in marasmic children. Clinical, pathological, and fine structural evaluation of the effect of protein-energy malnutrition and environmental contamination. American Journal of Clinical Nutrition. 1979; 32:1575–91.
 Lee P. Transient carbohydrate malabsorption and intolerance in diarrhea disease of infancy. In: Chronic Diarrhea of Children. E Lebenthal (Ed). Nestle, Vevey/Raven Press, New York, 1984.
 Stephen A. Effect of food on the intestinal microflora. In: Food and the Gut. J Hunter and V Jones (Eds.). Bailhere Tindall, London, 1985.
 Poley J. Ultrastructural topography of small bowel mucosa in chronic diarrhea in infants and children: Investigations with the scanning electron microscope. Chronic Diarrhea in Children. E Lebenthal (Ed). Nestle, Vevey/Raven Press, New York, 1984.
 Dvorak A, et al. Crohn’s disease: A scanning electron microscopic study. Human Pathology. 1979;10:165–77.
 Gottschall E. Breaking the Vicious Cycle: Intestinal Health Through Diet. Kirkton Press, Kirkton, Ontario, 2010.
 Galland L. Nutritional therapy for Crohn’s disease: disease modifying and medication sparing. Alternative Therapies 1999, 5:94-95.
 Nieves R., et al. Specific carbohydrate diet in treatment of inflammatory bowel disease. Tenn Med. 2004; 9:407.
 Olendzki B., et al. Pilot Testing a Novel Treatment for Inflammatory Bowel Disease. Clinical and Translational Science Research Retreat. 2011; May.
 Taus M., et al. New nutritional approach to inflammatory bowel disease: the nutraceuticals. Mediterr J Nutr Metab. 2009; 1:145–148.
 Takahashi H., et al. Usefulness of an elemental diet in Crohn’s disease. Inflammopharmacology. 2007; 15:15–17.
 Ogata H., et al. Does an elemental diet affect operation and/or recurrence rate in Crohn’s disease in Japan? J Gastroenterol. 2003; 38:1019–1021.
 Teahon K., et al. Ten years’ experience with an elemental diet in the management of Crohn’s disease. Gut. 1990; 31:1133-1137.
 Lochs H., et al. Comparison of enteral nutrition and drug treatment in active Crohn’s disease. Results of the European Cooperative Crohn’s disease study. IV. Gastroenterology. 1991;101:881–8.
 Hiwatashi N. Enteral nutrition for Crohn’s disease in Japan. Dis Colon Rectum. 1997 Oct; 40(10 Suppl):S48-53.
 Malchow H., et al. European Cooperative Crohn’s disease study: results of drug treatment. Gastroenterology. 1984; 86: 249-66.
 Singleton J., et al. NCCDS: adverse reactions to study drugs. Gastroenterology. 1979; 77: 870-83.
 Sylvester F. Appropriate use of corticosteroids in inflammatory bowel disease. In: Bayless T., Hanauer S., eds. Advanced Therapy of Inflammatory Bowel Disease. London: BC Decker; 2001:363-366.
 Present D. How to do without steroids in inflammatory bowel disease. Inflam Bowel Dis. 2000;1:48-57.
 Hanauer S. Aminosalicylates therapy for ulcerative colitis. In: Bayless T., Hanauer S., eds. Advanced Therapy of Inflammatory Bowel Disease. London: BC Decker; 2001:123-126.
 Borrelli O., et al. Polymeric diet alone versus corticosteroids in the treatment of active pediatric Crohn’s disease: a randomized controlled open-label trial. Clin Gastroenterol Hepatol. 2006;4(6):744-53.
 Kobayashi K., et al. Clinical usefulness of nutritional treatment for morphlogical findings of longstanding Crohn’s disease – especially focusing on comparison with drug treatment. Stomach Intest. 2004; 39:145–154.
“The Specific Carbohydrate Diet” and “SCD” are registered trademarks. Used with permission.