Strategies for Inflammatory Bowel Disease


A few weeks ago we discussed the concern that glutamine is potentially a bad idea in the context of inflammatory bowel disease (IBD).



You can read all about that here.


As a brief recap, it seems there is evidence supporting the idea that glutamine can worsen inflammatory bowel disease. There is also evidence suggesting it is beneficial.


Clinical data shows that glutamine is likely helpful in instances of severe acute trauma. But as severe as Crohn’s disease can be, we don’t have evidence suggesting that glutamine depletion occurs to the same degree.


Further, glutamine is abundant in protein dense foods. Assuming there is a slight increase in glutamine needs in inflammatory bowel disease, one is probably able to meet this need consuming an extra helping or two of protein daily.


That being said, you’re better off putting your energy and resources into other strategies for IBD. I’ve highlighted 4 considerations that are likely big needle movers in most cases.


Addressing Food Sensitivites

Saccharomyces Bouldardii




Addressing Dietary Sensitivities



IBD is characterized by dysregulation of the immune system. I like to call the immune system “homeland security,” a term I picked up from a medical doctor who practiced in Texas, Dr. Roby Mitchell. In IBD, homeland security is (in part) going after the wrong target, which happens to be tissues of the digestive tract. This can be the entire digestive track as is the case in Crohn’s, typically with sparing or the rectum. Or in the case of ulcerative colitis, the colon and rectum.


What is commonly recognized, is that there is ebb and flow to these conditions. Meaning that there are periods where the disease and symptoms are minimal and other periods where things are more severe. This is likely explained by inconsistent exposure to a trigger.


In some cases, certain components of food are likely to act as a trigger. Meaning you ingest a particular food, members of your homeland security spot components of that food, fire alarms are pulled and the downstream result is damage to your own tissues.


There is evidence supporting this idea. Studies have shown that 70-90% of folks can have their disease process arrested when subjected to a hypoallergenic diet [1, 2, 3, 4, 5].


Dietary triggers were determined in these studies by providing an elemental diet and reintroducing foods. An elemental diet is a nutritional formulation that has most of what the body needs, and is incredibly unlikely to be antigenic. In other words, it is nutrition that can be consumed in the context of IBD that is less likely to result in alarms being sounded.


What were the foods more frequently reported to be triggers?


Jones are friends reported in a study of 77 individuals [6] …



36% reacted to wheat

31% to dairy

20% to vegetables from the brassica family

16% to corn

14% to yeast

13% to tap water

13% to banana

10% to lamb and pork

10% to potato

7% to rice

4% to fish

3% to chicken, barley, rye, shellfish


Workman and pals in a similar type of study found [7] …


69% reacted to wheat

48% to dairy

31% to yeast

24% to corn

17% to potato

17% to tap water

14% to banana, tomato, wine and egg


In a different type of study. Riordon and friends achieved remission in 84% of patients using an elemental diet for 14 days. Those achieving remission were then split into a group receiving dietary therapy or steroid therapy. Median remission duration between groups was twice as long in the dietary therapy group [8]. The most frequent triggers in this group were (from most to least frequent):















Wheat, dairy and yeast seem to top the list in these three studies. Consideration of a trial without these components in the diet for some time seems reasonable in IBD. You’ll notice, looking at these lists, that many other commonly eaten food items are included. If one was to simply slash every suspicious food item, trouble could ensue. A diet consisting only of rice, lamb, cabbage or whatever ridiculous variant of an elimination diet to be tried can disrupt not only your physical health, but your psychological health as well.


I’ll be discussing the potentially disruptive nature of elimination diets in the future.


A safer strategy that is more effective long term is to remove what are likely the biggest offenders (grains and dairy). And swap your commonly eaten foods for alternatives.


Say your go to fruit is bananas, apples, and oranges. Maybe try mangos, strawberries, and pears for a few weeks.


You always do beef, chicken and pork? Try lamb, turkey, and bison.


Your starches are typically coming from potato, corn and rice? Maybe try swapping those out for yams and squash.


And so on…


The point here is that if you are reacting to food, it stands to reason that it is something you are regularly eating! This strategy of substitution is less daunting because you aren’t limiting yourself to a few food items.


And you are making it more likely you will be closer to your micronutrient and calorie requirements. This is incredibly important. Folks with IBD are generally wrought with wasting of lean mass and poor micronutrient status!


“But what if I eat mostly packaged foods?”


Then things get really tricky, and you need to become an expert label reader. Likelihood of success, also decreases substantially.


Still, you can learn what the major components of these packaged foods are and make appropriate substitutions. For instance, your go to snack bar is soft, chewy, comforting, dopamine surging Kellogg’s NutriGrain Bar. After reading the label so many times you are nauseated, you now know it’s primarily oats, wheat, corn syrup, peppered with some dairy. Some easy swaps- Lara Bars, Epic Bars or Vega Bars.


The principle is the same with other packaged foods. Doing potato chips with cottonseed oil? Try rice or bean chips with a different type of oil. Frozen dinners with beef or chicken, with potatoes and broccoli? Find a product with fish, rice and cauliflower.


Ideally, you wouldn’t be doing packaged foods with an ingredient list. But you are a human being with other obligations, other sources of stress and limited time.


If you’re frequently dining out, you have the least control over what you are exposed to and success is even more difficult to achieve. But some folks do pull it off…


Saccharomyces Boulardii



Saccharomyces Boulardii (S. Boulardii) is generally a non-pathogenic yeast available commercially in capsules and tablets. S. Boulardii doesn’t take up residence in the gut, but likely disrupts the harmful effects of pathogens that have taken up residence. You can read more about the specifics here [9].


Clinical data is sparse, but what is available suggests S. Boulardii can decrease frequency of diarrhea and relapse rates.


Plein and Hotz treated 20 individuals with S. Boulardii three times daily for two weeks noting a decrease in frequency of bowel movements and disease activity index in folks with stable Crohn’s disease. They then split these individuals into a group that would continue receiving S. Boulardii and a group that would get placebo for seven weeks. The group that continued treatment had a further decrease in bowel movement frequency and disease activity index. The placebo group’s bowel frequency and disease activity index returned to baseline levels [10].


In another study, investigators treated thirty individuals with stable Crohn’s disease using mesalamine alone or mesalamine + S. Boulardii. At 6 months out, relapse rates were 6% in the combination group versus 37.5% in the monotherapy group [11].


I stated S. Boulardii is generally not pathogenic. Not generally pathogenic in the sense that it is a disease-causing microorganism, but that it can potentially cause problems. Recall that clinical trials have found some folks IBD to be worsened by exposure to yeast, particularly saccharomyces cerevisiae. Further, the presence of anti-saccharomyces cerevisiae antibodies are highly specific to Crohn’s disease. Meaning that in some cases S. Boulardii could result in pulled fire alarms.


Dehydroepiandrosterone (DHEA)



Wait, what? Yes. DHEA. You should still maintain your sexual potency, even in the face of IBD!!! Kidding. No I’m not.


DHEA is a steroid hormone produced from cholesterol in the GI tract, brain, adrenals and gonads. It’s recognized as a weak androgen and precursor to our major androgens and estrogens. It’s typically used by clinicians to determine how much stress we’re under.


Relevant to what we are discussing, research suggests DHEA and further metabolites are helpful in IBD through their role in the regulation of your homeland security. How DHEA does this isn’t certain, but very recent investigation suggests that it may do so by dampening proinflammatory signaling [12].


DHEA has been found to be lower in folks with inflammatory bowel disease relative to healthy controls [13].


Andus and friends gave 20 patients with active inflammatory bowel disease for the past 6 months 200mg/day DHEA for 56 days. 14 patients responded favorably to treatment, with 12 going into remission based on indices of disease activity [14].


That is an awful lot. In this study, patients didn’t complain of excess hair growth, acne, oily skin… things one might expect from high doses of DHEA.


In his tome, Nutritional Medicine, Alan Gaby MD reports having success treating IBD patients with a much smaller dose of DHEA. 10-15mg/day per women and 15-20mg/day for men, particularly if their serum DHEA-sulfate levels (the form we typically measure) are at the lower end or below the reference range. Benefits were also noted in folks suffering from dermatomyositis and rheumatoid arthritis.


High dose DHEA may be helpful as a strategy to augment dietary modification and other therapies targeting IBD.





The status of many micronutrients is often harmed by IBD. An association between IBD and poor [insert micronutrient] status has been found.


This should make sense. Proteins that transport nutrients from our intestinal lumen and into our portal circulation or lymph are damaged by the inflammatory response. The brush border is often impaired, enzymatic secretions are suboptimal, meaning micronutrients are not optimally liberated from food. Further, an active disease process itself requires micronutrients to run the chemistry that fuels both carnage and repair.


A multivitamin is a frequent consideration. But not appropriate in every case.


Ulcerative Colitis tends to spare the small intestine. Sometimes the terminal ileum is involved, which is referred to as backwash ileitis. In an active disease process, one might expect oral B12 to be useless, since B12 is absorbed in the last few centimeters of the ileum.


Crohn’s disease includes the small intestine. It is most common for the terminal ileum to be involved, but frequently the jejunum and duodenum are also involved. Most micronutrients are absorbed in the jejunum. The implication here is the absorption of many micronutrients are likely impaired in Crohn’s disease.


I find it hard to believe that the jejunum in Ulcerative Colitis would maintain sufficient absorptive capacity, but who knows.


The point is, it may be helpful to hold off on oral micronutrients until an active disease process is arrested. While steps are being taken to dampen the inflammatory response with diet and other therapies, intravenous or intramuscular injections of micronutrients needed by the individual are likely helpful.


With the exception of Vitamin D, there is no clinical data supporting the use of micronutrients in IBD. One single study suggests Vitamin D modestly reduces relapse rates in Crohn’s disease [15].


Pulling everything together



The process of IBD can be arrested. The only strategy we have fairly decent evidence for is removing dietary triggers. But some of these other considerations may prove helpful.


Hypoallergenic diet. Strict elimination of grains and dairy. Substitution of commonly eaten foods with alternatives.


Saccharomyces Boulardii. Unfortunately, the authors don’t provide how many colony forming units were in each dose. The dosages in the studies I highlighted are in milligram quantity. It’s probably a good idea to start with a few billion colony forming units a titrate upward. Two good products are Jarrow Formulas and Klaire.


DHEA. 200mg/daily was used in the study cited above. Other studies have used similar amounts in systemic lupus erythematosus [16]. Dr. Alan Gaby’s suggestions (15-20mg/day women and 20-25mg/day for men) seem more reasonable.


Oral micronutrients specific to individual cases after the active process is arrested. Individualized intravenous or intramuscular nutrition during the active process. In both cases, you can find out exactly what you need working with an knowledgeable clinician.


In our next installment on IBD, we’ll be discussing two overlooked high-impact behaviors on the disease process that are certainly known to you, but are likely off your radar.


Side note: I make no money with the links to products I provide. They are products I have experience with and believe to be reliable.


Further Reading


[1] Ó’Moráin, C., et al. “Elemental diet in acute Crohn’s disease.” Archives of disease in childhood 58.1 (1983): 44-47


[2] Axelsson, Chr, and S. Jarnum. “Assessment of the therapeutic value of an elemental diet in chronic inflammatory bowel disease.” Scandinavian journal of gastroenterology 12.1 (1976): 89-95


[3] Hiwatashi, Nobuo. “Enteral nutrition for Crohn’s disease in Japan.” Diseases of the colon & rectum 40.10 (1997): S48-S53


[4] O’Morain C, Segal AW, Levi AJ. Elemental diet as primary treatment of acute Crohn’s disease: a controlled trial. Br Med J 1984;288:1859–1862.


[5] O’Morain C, Segal AW, Levi AJ. Elemental diets in treatment of acute Crohn’s disease. Br Med J 1980;281:1173–1175.


[6] Jones VA, Workman E, Freeman AH, et al. Crohn’s disease: maintenance of remission by diet. Lancet 1985;2:177–180.


[7] Workman EM, Jones VA, Wilson AJ, Hunter JO. Diet in the management of Crohn’s disease. Hum Nutr 1984;38A:469–473.


[8] Riordan AM, Hunter JO, Cowan RE, et al. Treatment of active Crohn’s disease by exclusion diet: East Anglian Multicentre Controlled Trial. Lancet 1993;342:1131–1134.


[9] Kelesidis, Theodoros, and Charalabos Pothoulakis. “Efficacy and safety of the probiotic Saccharomyces boulardii for the prevention and therapy of gastrointestinal disorders.” Therapeutic advances in gastroenterology 5.2 (2012): 111-125


[10] Plein K, Hotz J. Therapeutic effects of Saccharomyces boulardii on mild residual symptoms in a stable phase of Crohn’s disease with special respect to chronic diarrhea—a pilot study. Z Gastroenterol 1993;31:129–134.


[11] Guslandi M, Mezzi G, Sorghi M, Testoni PA. Saccharomyces boulardii in maintenance treatment of Crohn’s disease. Dig Dis Sci 2000;45:1462–1464.


[12] Alves, Vanessa Beatriz Freitas, et al. “Dehydroepiandrosterone (DHEA) restrains intestinal inflammation by rendering leukocytes hyporesponsive and balancing colitogenic inflammatory responses.” Immunobiology (2016)


[13] de la Torre B, Hedman M, Befrits R. Blood and tissue dehydroepiandrosterone sulphate levels and their relationship to chronic inflammatory bowel disease. Clin Exp Rheumatol 1998;16:579–582.


[14] Andus, T., et al. “Patients with refractory Crohn’s disease or ulcerative colitis respond to dehydroepiandrosterone: a pilot study.” Alimentary pharmacology & therapeutics 17.3 (2003): 409-414


[15] Mouli, Venigalla Pratap, and Ashwin N. Ananthakrishnan. “Review article: vitamin D and inflammatory bowel diseases.” Alimentary pharmacology & therapeutics 39.2 (2014): 125-136


[16] Sawalha, Amr H., and Susan Kovats. “Dehydroepiandrosterone in systemic lupus erythematosus.” Current rheumatology reports 10.4 (2008): 286-291


[17] Gaby, Alan R. “Nutritional medicine.” JAMA 306.20 (2011)



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