Chapter 2

Crohn’s disease exclusion diet (CDED)

The CD exclusion diet (CDED), is a whole-food diet coupled with PEN [partial enteral nutrition], designed to reduce exposure to dietary components, hypothesized to negatively affect the microbiome (dysbiosis), intestinal barrier, and intestinal immunity. It has shown promising ability to induce remission and decrease inflammation in case series in both children and adults with CD, including in patients with secondary loss of response to anti-tumor necrosis factor therapy.  ~Levine et al., 2019

The CDED, which avoided or reduced exposure to animal fat, dairy products, gluten, and emulsifiers and enabled exposure to fiber from fruits and vegetables led to remission in 70% of patients, primarily in patients with early mild-to moderate disease.  ~Sigall-Boneh et al., 2014, emphasis added

CDED is a long-term strategy that may be used as monotherapy, as combination therapy, for de-escalation of drugs, and as a rescue therapy for refractory patients.  ~Herrador-López et al., 2010

_______________________________________________________________________

When it comes to diets for IBD, the diet we will now discuss is a dandy—highly effective in taking an individual from active disease to remission, and in a matter of weeks.  The diet is called the Crohn’s Disease Exclusion Diet, or CDED for short.  Although designed with the Crohn’s patient in mind, perhaps the ulcerative colitis patient should pay attention and learn a lesson or two.  Particularly so, since it is possible for a patient to be first diagnosed as having ulcerative colitis and later to have the diagnosis changed to Crohn’s (Guindi and Riddell, 2004; Moss and Cheifetz, 2008).  For the individual with ulcerative colitis, being knowledgeable about the CDED just might come in handy later on down the line.

The CDED has been in use, informally, for quite some time.  It is basically the combination of enteral nutrition and real, solid food.  Anna (of the last chapter) was on it, or at least sort of on it, after she transitioned from EEN to PEN plus solid food.  But with CDED, this whole business has been fine-tuned to achieve a greater degree of success, and currently goes by the name ModuLifeTM.  The solid-food part is an exclusion diet, designed to reduce or eliminate exposure to foods and dietary components which negatively affect both the microbiome and intestinal barrier function—all packaged in a program that transitions an individual from an initial phase to an intermediate phase, then on to a maintenance phase.  It even comes with a nifty little app!  It’s almost like you can’t screw this up.  (I’m holding my breath.)

In a nutshell:

The Crohn Disease Exclusion Diet (CDED) is a whole food diet that can be combined with PEN. Specifically, gluten, dairy products, gluten-free baked goods and breads, animal fat, processed meats, products containing emulsifiers, canned goods, and all packaged products with a due date are not allowed during the initial period. It does allow specific spices and herbs, whereas all other condiments and sauces are not permitted. Up to 18 to 20 g of fibre per day can be consumed. In the second 6-week period, a fixed portion of whole grain bread is allowed as are small amounts of nuts, fruits, legumes and vegetables. Patients with strictures should continue quantitative restriction of fruits and vegetables on an individual basis.  (Wellens et al., 2021)

To see it all in action, let’s take a look at a handful of case reports.

 

Case report: Levi

Levi, 18 years of age, presented with a three-month history of the usual—abdominal pain, weight loss, intermittent diarrhea.  His C-reactive protein (CRP) and fecal calprotectin, laboratory tests that help measure disease activity in IBD, were both off the charts (meaning very high).  Endoscopy was performed and revealed ulcers in the duodenum, ileum, and colon.  Biopsies identified chronic inflammation in the ileum as well as the presence of what are called granulomas.  Taken together, the diagnosis of Crohn’s disease was an easy diagnosis to make.  And from the sound of things, Levi was in a lot of trouble.

Treatment options were discussed with Levi and his parents, which included the potential use of biologic therapy.  And in Levi’s case, a biologic may not have been a bad idea at all.  However, and for reasons not discussed in the report, Levi’s parents said, “no way” and wanted to take things in a different direction.  Since the biologic avenue was blocked by parental refusal, and his physician was aware of a treatment option available that the parents might find acceptable, Levi was referred to a physician who was experienced in using nutrition to treat Crohn’s.

“So how did it go?”  Thanks for asking.  Short answer: It went very well.

Levi was started on the CDED program, which included PEN, and after six weeks, he was in clinical remission.  His CRP and fecal calprotectin level both returned to normal.  “The patient transitioned to the phase 3 maintenance diet without drugs and remained in remission during the year.”  Fifteen months after beginning the CDED program, a colonoscopy was performed and “demonstrated complete mucosal healing.”  Furthermore, biopsies from the colon were normal, and ileal biopsies demonstrated only “mild focal active inflammation.”

All things considered, it looks like CDED was a good call.  I hope the mild inflammation goes away and goes away soon.  However, Levi may need a medication or two to help him maintain his remission.

Reference:

Levine A, El-Matary W, Van Limbergen J. A Case-Based Approach to New Directions in Dietary Therapy of Crohn’s Disease: Food for Thought. Nutrients. 2020 Mar;12(3):880.

 

Case report: Julia

At the tender age of 10, Julia was experiencing ongoing abdominal pain in addition to weight loss—losing nearly 4 ½ pounds over a period of 3 months.  She finally made it in to see a gastroenterologist.  Her workup identified elevated CRP and fecal calprotectin levels, and a colonoscopy revealed ulcers in both transverse and ascending colon, the ileum unaffected.  Biopsies of the affected portions of the colon indicated that inflammation had been present for quite some time.  For how long, no one really knows.  Based on the findings, the diagnosis of Crohn’s disease was easy to make.  Julia’s pediatric disease activity index (PCDAI) was 30 (remission defined as below 10), indicating her disease was in the moderately active range.

Perhaps sensing there was something else more agreeable than drug therapy, perhaps safer and more effective, Julia declined the offer of conventional therapy and agreed to follow a proposed alternative, the CDED plus PEN program.

After six weeks she was in clinical remission with normal CRP and had regained 1.3 kg. She performed the second phase of the induction diet and then the phase 3 maintenance diet. During the subsequent 12 months remained in clinical remission with normal CRP and fecal calprotectin.  (Levine et al., 2020)

There is more:

An MRE and colonoscopy were repeated between 12–15 months, both were completely normal at this time. She remained in sustained deep remission for three years, maintaining the diet with some difficulty as she struggled with adherence at times. During the ensuing summer she travelled abroad several times and did not adhere to the diet. Though she felt well her calprotectin increased from 16 to 300 µg/g. She regressed to the phase 1 induction diet for four weeks and then returned to the maintenance diet. Her calprotectin normalized and a subsequent ileocolonoscopy was completely normal.  (Levine et al., 2020)

Well, that went well.  But Julia may need ongoing adherence to the CDED plus PEN program to maintain her remission.  Indeed, after three years following the CDED, she stopped the diet and paid the price.  Although she felt well, her calprotectin once again became elevated, indicating that her disease had been reactivated.  Subsequently, Julia returned to phase 1 of the diet for a period of four weeks, followed by the maintenance phase.  A repeat calprotectin level returned to normal and Julia lived happily ever after.

Reference:

Levine A, El-Matary W, Van Limbergen J. A Case-Based Approach to New Directions in Dietary Therapy of Crohn’s Disease: Food for Thought. Nutrients. 2020 Mar;12(3):880.

 

Case report: Liam

Well, you can’t put things off forever, but Liam, age 15, tried his best.  Although he was experiencing Crohn’s to the fullest, there was an unexplained delay in seeking medical attention.  Finally, after being “visited” with an acute flare of his chronic abdominal pain, diarrhea, and rectal bleeding, it was time (past time) to go see the doctor.  And now he was running a fever.  He had also experienced significant weight loss and appeared to be anemic.  His workup included labs, imaging studies, and endoscopy.  Crohn’s disease, producing ulceration and narrowing of his terminal ileum, became the primary diagnosis.

As if Crohn’s wasn’t bad enough, imaging studies also revealed Liam had developed an entero-enteral fistula (an abnormal passageway between one segment of the bowel to another).  But there was more.  He had also developed two abscesses, one associated with the fistula, the other located in the abdomen and easily accessible through the skin.  For the latter, a drainage tube was placed.  And if that wasn’t enough, also identified was a fistula involving the internal anal sphincter (of Liam).  Liam, apparently, does not fool around.  When he has a hideous disease, he goes all out.

Treatment included EEN, antibiotics, and infliximab.

After a few weeks, on the above therapy, imaging studies showed marked improvement and the drainage tube was removed.  After eight weeks, Liam was placed on CDED plus PEN, replacing EEN.  “After four months, MRE showed resolution of penetrating ileal disease without evidence of a fistula . . ..”  Liam’s response to therapy was impressive, indeed.  “At the latest clinical follow-up, perianal disease was quiescent without a visible external fistula or drainage.”

And did you notice?  Liam did not require surgery.  I am impressed.  Are you?  But is Liam out of the woods?  It is just too soon to tell.  I hope he will continue following the CDED program and continue with whatever drug therapy that may be prescribed to control his disease.  I’m still a little worried about Liam.

Reference:

Levine A, El-Matary W, Van Limbergen J. A Case-Based Approach to New Directions in Dietary Therapy of Crohn’s Disease: Food for Thought. Nutrients. 2020 Mar;12(3):880.

 

Case report: Abel

Abel was diagnosed with Crohn’s disease at the age of 13.  He is now 16.  And the past three years have not been very kind to him.  His Crohn’s is now extensive, like all-over-the-place extensive, and included perianal disease.  Despite aggressive medical care, Abel was “a non-responder.”  Powerful meds, such as azathioprine (Imuran) and methotrexate, did not stem the tide, and neither did infliximab (Remicade), adalimumab (Humira), or ustekinumab (Stelara).  It became increasingly evident that surgery was the only option available and was promptly placed under consideration.  But fate would step in, making surgery unnecessary.

Before a final decision could be made or a surgery date met, Able was hospitalized with a severe flare of his disease.  In as much as he had a history of not responding to drug therapy, perhaps there was nowhere else to turn than turn to nutritional therapy.  He was placed on EEN for two weeks, followed by CDED with PEN for the following 10 weeks.

By the third week he was asymptomatic for the first time in eight months. At week 6, his CRP had declined from 120 to 29 g/L, his albumin had increased from 33 to 42 g/L, and his PCDAI had declined from 47.5 to 5. His calprotectin was repeated at week 14 and it had declined from 1300 to 263 µg/g. He is continuing on ustekinumab 90 mg every eight weeks with the maintenance diet and, at this time, five months have elapsed and he is still in remission.  (Levine et al., 2020)

 From Abel’s experience, we learn that diet may come to the rescue of even difficult cases.  And most importantly, it can make the physician look like he or she is at the top of their game.

Reference:

Levine A, El-Matary W, Van Limbergen J. A Case-Based Approach to New Directions in Dietary Therapy of Crohn’s Disease: Food for Thought. Nutrients. 2020 Mar;12(3):880.

 

The ModuLifeTM life

 The recently described CDED is a whole-food diet coupled with PEN (MODULEN™ IBD, Nestlé). CDED is a structured diet designed to reduce exposure to dietary components that may negatively affect the microbiome, intestinal barrier, and intestinal immunity. CDED limits exposure to animal fat, certain types of meat, gluten, maltodextrin, emulsifiers, sulfites, and certain monosaccharides.  ~Verburgt et al., 2021

CDED, unlike EEN, constitutes a long-term strategy for maintaining remission and is nutritionally balanced. By including dietary fiber, CDED corrects the bacterial dysbiosis present in these patients, and is therefore a much more realistic and advanced approach than EEN if complied with adequately.  ~Herrador-López et al., 2010

 It then remains important to position diet as a sustainable lifestyle intervention, used in combination with drugs when needed—not simply to avoid drugs.  ~Levine et al., 2019

The CDED plus PEN, an approach that became known as ModuLifeTM, works for Crohn’s because it addresses several factors that help establish and perpetuate the disease.  First, it restricts or excludes foods and dietary components that are known to promote intestinal inflammation.  Second, it reduces “leaky gut”—thereby reducing the bacterial challenge that requires an ongoing, aggressive immune response to control all the madness.  Third, it delivers generous amounts of dietary fiber, correcting a deficiency that “may cause catabolism [degradation] of the mucous layer, leading to increased permeability of the mucous layer, and allowing increased contact between luminal bacteria and the epithelium.”  (Levine et al., 2018)  Fourth, it provides nutrients and other factors directly to the intestinal lining.  And finally, it improves bacterial clearance from affected tissues.  And although restrictive, the ModuLifeTM program allows considerable variation, which promotes compliance.  And in the maintenance phase, you are allowed to cheat a day or two each week and pretend to be a normal person.  So, what is life like on the ModuLifeTM program?

A day in the life

The ModuLifeTM program has three distinct phases, as follows:

Phase 1 of the diet is the most restrictive and lasts for a period of 6 weeks.  During this phase, you eliminate or greatly restrict foods and food components that promote inflammation or otherwise offend—such as foods containing animal fats, dairy products, gluten, and emulsifiers, as previously mentioned.  In addition, during Phase 1, foods high in dietary fibers are restricted to prevent bowel obstruction from occurring should stricturing disease be present.  Meat is wisely withheld for the first 6 weeks, but fish is allowed in limited amounts.  To make up for missing calories brought about by food restriction, as well as to provide additional health-promoting factors, enteral nutrition is added to meet 50% of the individual’s caloric needs.

Phase 2 is more liberal, and also of 6 weeks duration.  Life is better during Phase 2.  You get to eat from an expanded list of allowed foods, with restrictions still placed on meat and fish, and you decrease your Modulen® intake by half, meeting 25% of your caloric needs with liquid nutrition.  Theory has it, the Modulen® supplies the intestine with good things it might otherwise miss out on, as well as guaranteeing that a significant portion of the diet is kind and gentle to the intestinal tract.

Phase 3, or maintenance phase, is where life begins anew.  You are now normal (or so you think), but not so normal as to allow you to resume your previous dietary choices and previous dietary habits.  You continue life on the ModuLifeTM program by eating foods from the approved list and by consuming 25% of your calories from PEN (Modulen® or Modulen IBD® preferred).  And during this phase, you are allowed to cheat on the diet, but cheat only a little.

 The Maintenance Phase requires five contiguous days following the diet as written, then allows for a maximum of two contiguous days (generally weekends) that allow two free meals per day (maximum of four free meals per week), excluding only hot dogs, sausages, soft drinks, luncheon meats, bacon, and frozen dough from those free meals.  (Crohn’s Disease Exclusion Diet (ntforibd.org))

“So,” you ask, “What does a typical day on Phase 1 look like?”  Let’s ask Herrador-López and colleagues (see Herrador-López et al., 2020).  They seem nice.  I’m sure they can help us out.

According to Herrador-López and colleagues, and by way of example, Phase 1 looks something like this: For breakfast, you eat 3 banana pancakes and drink 250 ml’s of Modulen®.  Sometime before lunch you drink 250 ml’s of Modulen® as a snack.  For lunch, it is homemade potato chips, along with chicken meatballs and homemade tomato sauce, and a banana.  Next is an afternoon snack.  You get creative and blend an apple with 350 ml’s of, you guessed it, Modulen®.  Then you drink your creation.  For dinner, you eat baked chicken breast, along with baked potato and carrot.  All you can say is “Yummy!”  (Try to mean it.)

Again, by way of example, according to Herrador-López and colleagues, Phase 2 goes something like the following: For breakfast, you eat a slice of wholewheat toast topped with olive oil and tomato slices, along with sipping Modulen®, 250 ml’s.  Your mid-morning snack is Modulen®, again 250 ml’s, along with a carrot oat muffin or two.  For lunch, you eat a chickpea and tuna salad, a hard-boiled egg, 1/3rd of an avocado, and 1/2 of a sweet potato, followed by a banana.  (You must really be hungry.)  Your mid-afternoon snack is sliced apple with almond butter.  When dinner arrives, you eat a homemade beef burger, homemade potato chips, a potato, and a banana.  Then it’s on to Phase 3.

According to Herrador-López and colleagues, Phase 3, the maintenance phase, looks a lot like this: For breakfast, you eat a slice of wholewheat toast topped with olive oil and tomato slices, along with  Modulen®, 250 ml’s.  Your mid-morning snack is once again Modulen®, 250 ml’s, along with a pear.  Lunch follows, and is quinoa salad with tomato and onion, grilled salmon, and an apple.  For your mid-afternoon snack, you eat a serving of yogurt.  For dinner, it’s a Spanish omelet, to include tomato and onion, a serving of roasted peppers, and yet another banana.

So, as you can see, the ModuLifeTM program is doable (and filling).  It may be the best diet option available for the patient with Crohn’s.

For detailed information on the Crohn’s Disease Exclusion Diet (CDED), particularly covering the foods that are mandatory, the foods that are allowed, and the foods that are disallowed, search for the article entitled Crohn’s Disease Exclusion Diet (CDED) by name or follow this URL: https://ntforibd.org and look under the Therapeutic Diets tab.  Another excellent resource on the ModuLifeTM program is: Introducing ModuLifeTM: An Innovative Dietary Management Approach for Crohn’s Disease.  You can find it at https://www.modulife.us/patients.  Both articles are mandatory reading, so don’t skip this assignment.  You’re in enough trouble already.

 

References

Crohn’s Disease Exclusion Diet (CDED) Crohn’s Disease Exclusion Diet (ntforibd.org)

Di Caro S, Fragkos KC, Keetarut K, Koo HF, Sebepos-Rogers G, Saravanapavan H, Barragry J, Rogers J, Mehta SJ, Rahman F. Enteral nutrition in adult Crohn’s disease: Toward a paradigm shift. Nutrients. 2019 Sep;11(9):2222.

Guindi M, Riddell RH. Indeterminate colitis. Journal of Clinical Pathology. 2004 Dec 1;57(12):1233-44.

Herrador-López M, Martín-Masot R, Navas-López VM. EEN Yesterday and Today… CDED Today and Tomorrow. Nutrients. 2020 Dec;12(12):3793.

Levine A, Boneh RS, Wine E. Evolving role of diet in the pathogenesis and treatment of inflammatory bowel diseases. Gut. 2018 Sep 1;67(9):1726-38.

Levine A, Wine E, Assa A, Boneh RS, Shaoul R, Kori M, Cohen S, Peleg S, Shamaly H, On A, Millman P. Crohn’s disease exclusion diet plus partial enteral nutrition induces sustained remission in a randomized controlled trial. Gastroenterology. 2019 Aug 1;157(2):440-50.

Levine A, El-Matary W, Van Limbergen J. A Case-Based Approach to New Directions in Dietary Therapy of Crohn’s Disease: Food for Thought. Nutrients. 2020 Mar;12(3):880.

Moss AC, Cheifetz AS. How often is a diagnosis of ulcerative colitis changed to Crohn’s disease and vice versa?. Inflammatory bowel diseases. 2008 Oct 1;14(suppl_2):S155-6.

Sigall-Boneh R, Pfeffer-Gik T, Segal I, Zangen T, Boaz M, Levine A. Partial enteral nutrition with a Crohn’s disease exclusion diet is effective for induction of remission in children and young adults with Crohn’s disease. Inflammatory bowel diseases. 2014 Aug 1;20(8):1353-60.

Triantafillidis JK, Vagianos C, Papalois AE. The role of enteral nutrition in patients with inflammatory bowel disease: current aspects. BioMed research international. 2015 Jan 1;2015.

Verburgt CM, Ghiboub M, Benninga MA, de Jonge WJ, Van Limbergen JE. Nutritional Therapy Strategies in Pediatric Crohn’s Disease. Nutrients. 2021 Jan;13(1):212.

Wellens J, Vermeire S, Sabino J. Let Food Be Thy Medicine—Its Role in Crohn’s Disease. Nutrients 2021, 13, 832.

~ Preface ~

Treatments for IBD [inflammatory bowel disease] in clinic cause big side effects. Their aims are ambiguous and they are costly. Their curative effects are not satisfying. ~Jian et al., 2005

Likely, you have Crohn’s, or perhaps it is ulcerative colitis that is holding you tightly within its grip. If I were to venture a guess, you have had enough and are looking for a way out. And in a personal quest to achieve remission and return to a normal life, you find yourself holding a certain book in your hands, this book. Which leads us to a couple of good questions, “Why was this book written?” and “How can this book help me?”

I, too, am on a personal quest. During my career as a Registered Nurse, I noticed something both glaring and most unfortunate, something that clearly needed to be addressed. I noticed a category of patients who know so little about the disease they have. I also noticed that this knowledge deficit is not without negative consequences. So, I set out to do something about it. This quest, this journey, soon became a passion and has consumed over a decade of my life. During this interval of time, I have written two books, and now a third, with the goal of helping those suffering from Crohn’s disease and those suffering from ulcerative colitis—offering insight and exploring options.

Along the way, I noticed something else. I noticed that physicians, too, need a little help here—so much to learn, so much to consider, so many things set aside or otherwise obscured from view. So, this book is for the physician, too. In a world where the emphasis is placed on drug therapy, a therapy that does great things but can fail and even harm, there is a clear need for options and backup plans in the battle against Crohn’s and the battle against ulcerative colitis.

Modern IBD management has been revolutionized by the introduction of antitumor necrosis factor alpha (antiTNFα) medications (eg, Infliximab and Adalimumab). These drugs,

however, are not without cost or risk. For many patients, price or side effect may prohibit a long-term successful course of therapy. In these patients, alternative means of lowering serum TNFα would be highly desirable. (Kolcun et al., 2017)

And perhaps you have learned a lesson or two the hard way and want to minimize the danger.

Cortiocosteroids have short-term side effects of weight gain, emotional liability, glucose intolerance, and risk of secondary infections, especially fungal. Acute complications with some immunomodulators (azathioprine, 6-mercaptopurine) include idiopathic pancreatitis and neutopenia. Acute allergic reactions have been reported with the new anti-TNF-α compounds; these drugs can also increase the risk of reactivation of tuberculosis and induce a lupus-like reaction, serum sickness syndrome, and/or anaphylaxis. (Smith et al., 2007)

So, I have written a book just for you. In this book, I give example after example of individuals who have achieved remission using alternative and complementary measures, including the use of drugs that are not typically used in the battle against Crohn’s and ulcerative colitis, drugs used for something else but may be a safer option. With few exceptions, the examples given here are from actual case reports found in medical literature. And as I like to say, “If remission can happen to them, there is a good chance it can happen to you.”

But I must warn you, this is not a do-it-yourself instruction manual. To play it safe, you will need to work with a physician each step of the way. So, promise me you will discuss any path you wish to follow with your physician, to first gain approval and then to secure cooperation. Besides, except for the use of diet or supplements, you will need a prescription for most of the therapies we will discuss. And to be safe, expert guidance is always essential with any form of therapy you choose to adopt.

One more thing before we move on. The names used in the case reports included in the book are all made up, with few exceptions. For reasons of privacy, the actual names of individuals in medical reports are not given. But I felt that by adding a name to the report, this would make the story more relatable as well as easier to tell. And don’t forget, these are real people! Real people have real names, or in this case, real fake names. Does this all make sense?

Now, with the preliminaries out of the way, we can begin our journey together and explore the possibilities.

Introduction

While case reports are assigned limited level of evidence and are unable to deliver quantitative data, they still provide practical clinical real- world facts and are still indispensable for broadening medical knowledge. ~Scarallo et al., 2021

I’ve always liked stories.     I’ve always liked to tell stories.      And I especially like telling the stories I have included in the pages of this book. I hope you will listen. I hope you will learn the valuable lessons they contain. They are stories worth sharing.

With few exceptions, the stories I tell are stories that have already been told. They are case reports that can be found scattered throughout medical literature, perhaps waiting for someone to gather them up, dust them off, organize them in an orderly fashion, and retell them in a manner that all can understand. Now why would I feel the need to put forth such an effort?

Stories of success not only give us hope, hope that difficult situations can be overcome, and point to paths that may be worth traveling. And in the case of Crohn’s and ulcerative colitis, two diseases that have claimed millions of victims and are exceptionally difficult to defeat, we need all the weapons we can add to our arsenal to achieve victory, one individual at a time. And, as you will soon discover, there are many weapons available from which to choose.

As we explore the options, I will look for opportunities to teach you valuable lessons about the disease you have, whether it be Crohn’s or ulcerative colitis, and I’ll start with the gray box that follows. And I promise, I won’t overwhelm you. Here, I will teach you the easy stuff. And all the while, I will try to entertain you a little, so you don’t fall asleep. You can thank me later.

I sense your eagerness to get right to it, so I will end the beginning with this:

While case reports are assigned limited level of evidence and are unable to deliver quantitative data, they still provide practical clinical real-world facts and are still indispensable for broadening medical knowledge. They provide an in-depth understanding of each individual case as opposed to large research studies with their “nomothetic approach.” Indeed, a case report is the only way to describe in details any unusual observations regarding symptoms, medical history, clinical findings, course of disease, pharmacological and non-pharmacological interventions and their complications, associations of diseases, side effects of drugs, etc. Consequently, a case report is a major educational tool that can inform readers on new observations, generate hypotheses, and facilitate detection of similar or identical cases. (Scarallo et al., 2021)

In essence

Both ulcerative colitis and Crohn’s disease are characterized by the disruption of the epithelial cell barrier and the dysfunction of the immune system. Disruption of the intestinal epithelial barrier in IBD allows the invasion of commensal bacteria. This leads to influx of inflammatory cells and their constant activation. ~Kristek and Loscher, 2014, emphasis added

While everything IBD is so complex, it is not all that difficult to understand what is basically going on. And it might be helpful to be in the know. So, here you go!

In the past, we were told that Crohn‘s and ulcerative colitis were autoimmune diseases. You can promptly dismiss this notion. Neither one is an autoimmune disease. They are something else.

More recently, and in the present, Crohn‘s disease and ulcerative colitis are characterized as diseases caused by a disordered (aberrant) reaction by the immune system to normal intestinal bacteria. While this theory may answer some questions, and undoubtedly aberrancy against intestinal bacteria does occur in both diseases, there is something clearly more fundamental in play that would answer the question,

“What is it that I have?” Here, I’ll do my best to explain.

In Crohn’s disease, the immune system has a serious problem dealing with bacteria that have arrived within the tissues and cells of the gut. Normally, this should not occur to any relevant degree, other than minor incursions that are quickly resolved. But due to genetic defects or unfavorable circumstances, the immune cells are unable to properly defend against and clear invasive bacteria, making Crohn’s an immunodeficiency disease which allows bacteria to persist within tissues and inside of cells. In support,

The notion that Crohn’s disease occurs as an aberrant reaction to commensal (typically present) microbiota in genetically susceptible hosts is widely regarded by physicians as fact. Yet although it is undisputed that Crohn’s disease is immune-mediated, an aberrant reaction to one’s own native flora is far from proven. (Campbell et al., 2012)

A substantial body of data has emerged in recent years to suggest that the primary defect in Crohn’s disease is actually one of relative immunodeficiency. (Marks et al., 2010)

And in Crohn’s, an immune cell called the macrophage is particularly defective in its role of clearing bacteria that have breached the layers of defense.

Recent work provides evidence of a failure of acute inflammation in Crohn’s disease (CD), and suggests that the primary defect operates at the level of the macrophage and cytokine release.

CD (Crohn’s disease) is a complex disease comprising multiple stages and phenotypes. We recently demonstrated that CD patients clear bacteria less rapidly than control individuals, which was associated with delayed recruitment of neutrophils and defective macrophage function. (Sewell et al., 2012, emphasis added)

When macrophages in the inflamed intestine show an enhanced pro-inflammatory phenotype, their ability to eradicate intracellular pathogens is decreased as their phagocytosis is significantly reduced. This probably accounts for recurrent infection in IBD Patients with pathogens that target macrophages, such as Mycobacterium paratuberculosis. (Kristek and Loscher, 2014, emphasis added)

Compared with Crohn’s, ulcerative colitis is less complex at its core. Ulcerative colitis occurs as the result of an immune response to bacteria that have breached the mucus layer of defense and colonize the surface of the rectum, and then colonize onward and upward to involve the colon, perhaps the entire colon.

Normally, luminal bacteria in the gut are withheld from contact with the epithelium by an adherent mucus layer, but in UC the bacteria reside on the luminal surface where they probably induce and maintain the inflammatory process. (Schneider et al., 2010, emphasis added)

Once damaged, the barrier is unable to exclude highly immunogenic fecal bacterial antigens [immune stimulating bacterial components] from invading the normally sterile submucosa. (Pravda, 2005)

In ulcerative colitis, it becomes obvious as to why all the inflammation is occurring. Bacteria are living where they should not be, and an ongoing immune response is necessary . . . and things spiral out of control.

I thought you would benefit from knowing my views on the fundamental nature of both Crohn’s and ulcerative colitis. But regardless of the fundamental cause, I clearly recognize that inflammation begets inflammation. So, efforts to control inflammation, be it with drugs or by other treatment modalities, can help turn things around and head the patient in the right direction, regardless of a specific cause.

I will conclude with this:

Although loss of tolerance to the gut microbiota [microbes] is demonstrated in animal models of inflammatory bowel disease, there is only limited evidence for this finding in patients with

Crohn’s disease and none in those with ulcerative colitis. (Danese and Fiocchi, 2011, emphasis added)

 

Clues

There are a few laboratory tests that you will find mentioned from time to time in the book. And since you are eager to learn, I will summarize the three most common ones here.

A CRP is a test that measures the concentration in the blood of a molecule called C-reactive protein, a molecule normally released during inflammation. Elevated values suggest the degree of disease severity. The higher the number, the greater the disease activity.

An ESR is a test that measures, in a standardized way, how fast red blood cells fall and settle at the bottom of a laboratory tube. Because inflammation promotes red blood cell clumping, and clumps of red blood cells fall faster than non-clumped red blood cells, an estimate of the degree of inflammation can be obtained. In this test, an abnormally high value indicates an inflammatory process is occurring somewhere in the body.

Finally, a Fecal Calprotectin is a test that measures the amount of calprotectin accumulating within the stool. Calprotectin is a molecule involved in the mobilization of a white blood cell type, the neutrophil, to sites of inflammation. An elevated fecal calprotectin level suggests intestinal inflammation is occurring, with a higher level inferring a higher degree of inflammation.

 

Basic terms and concepts

To better understand what is being said, there are a few terms and concepts that you will need to become familiar with as we continue.

The most relevant are:

Inflammation—a cell or tissue response to a threat such as injury or bacterial invasion, and is generally characterized by redness, pain, and swelling. It involves changes in metabolism and cellular behavior, as well as the production of specific molecules (complex proteins called cytokines) used to orchestrate the inflammatory response, a response that should defeat the enemy and lead to resolution (healing).

Cytokine—a regulatory protein produced by a cell for the purpose of promoting or decreasing an inflammatory response or influencing other cellular activity. For example, TNF-α and IL-10 are cytokines that act to increase the inflammatory response or decrease the inflammatory response, respectively. A cytokine produced by one cell may act locally, regionally, systemically, or even act on the cell of origin.

Inflammatory pathway—a series of cellular mechanisms that coordinate with each other to initiate and sustain a particular aspect of the inflammatory response. The inflammatory response is highly regulated. This requires cellular mechanisms that both activate or restrain a particular series of events that will increase

Preface

~ Preface ~

Treatments for IBD [inflammatory bowel disease] in clinic cause big side effects. Their aims are ambiguous and they are costly. Their curative effects are not satisfying. ~Jian et al., 2005

Likely, you have Crohn’s, or perhaps it is ulcerative colitis that is holding you tightly within its grip. If I were to venture a guess, you have had enough and are looking for a way out. And in a personal quest to achieve remission and return to a normal life, you find yourself holding a certain book in your hands, this book. Which leads us to a couple of good questions, “Why was this book written?” and “How can this book help me?”

I, too, am on a personal quest. During my career as a Registered Nurse, I noticed something both glaring and most unfortunate, something that clearly needed to be addressed. I noticed a category of patients who know so little about the disease they have. I also noticed that this knowledge deficit is not without negative consequences. So, I set out to do something about it. This quest, this journey, soon became a passion and has consumed over a decade of my life. During this interval of time, I have written two books, and now a third, with the goal of helping those suffering from Crohn’s disease and those suffering from ulcerative colitis—offering insight and exploring options.

Along the way, I noticed something else. I noticed that physicians, too, need a little help here—so much to learn, so much to consider, so many things set aside or otherwise obscured from view. So, this book is for the physician, too. In a world where the emphasis is placed on drug therapy, a therapy that does great things but can fail and even harm, there is a clear need for options and backup plans in the battle against Crohn’s and the battle against ulcerative colitis.

Modern IBD management has been revolutionized by the introduction of antitumor necrosis factor alpha (antiTNFα) medications (eg, Infliximab and Adalimumab). These drugs,

however, are not without cost or risk. For many patients, price or side effect may prohibit a long-term successful course of therapy. In these patients, alternative means of lowering serum TNFα would be highly desirable. (Kolcun et al., 2017)

And perhaps you have learned a lesson or two the hard way and want to minimize the danger.

Cortiocosteroids have short-term side effects of weight gain, emotional liability, glucose intolerance, and risk of secondary infections, especially fungal. Acute complications with some immunomodulators (azathioprine, 6-mercaptopurine) include idiopathic pancreatitis and neutopenia. Acute allergic reactions have been reported with the new anti-TNF-α compounds; these drugs can also increase the risk of reactivation of tuberculosis and induce a lupus-like reaction, serum sickness syndrome, and/or anaphylaxis. (Smith et al., 2007)

So, I have written a book just for you. In this book, I give example after example of individuals who have achieved remission using alternative and complementary measures, including the use of drugs that are not typically used in the battle against Crohn’s and ulcerative colitis, drugs used for something else but may be a safer option. With few exceptions, the examples given here are from actual case reports found in medical literature. And as I like to say, “If remission can happen to them, there is a good chance it can happen to you.”

But I must warn you, this is not a do-it-yourself instruction manual. To play it safe, you will need to work with a physician each step of the way. So, promise me you will discuss any path you wish to follow with your physician, to first gain approval and then to secure cooperation. Besides, except for the use of diet or supplements, you will need a prescription for most of the therapies we will discuss. And to be safe, expert guidance is always essential with any form of therapy you choose to adopt.

One more thing before we move on. The names used in the case reports included in the book are all made up, with few exceptions. For reasons of privacy, the actual names of individuals in medical reports are not given. But I felt that by adding a name to the report, this would make the story more relatable as well as easier to tell. And don’t forget, these are real people! Real people have real names, or in this case, real fake names. Does this all make sense?

Now, with the preliminaries out of the way, we can begin our journey together and explore the possibilities.

Introduction

Introduction

While case reports are assigned limited level of evidence and are unable to deliver quantitative data, they still provide practical clinical real- world facts and are still indispensable for broadening medical knowledge. ~Scarallo et al., 2021

I’ve always liked stories.     I’ve always liked to tell stories.      And I especially like telling the stories I have included in the pages of this book. I hope you will listen. I hope you will learn the valuable lessons they contain. They are stories worth sharing.

With few exceptions, the stories I tell are stories that have already been told. They are case reports that can be found scattered throughout medical literature, perhaps waiting for someone to gather them up, dust them off, organize them in an orderly fashion, and retell them in a manner that all can understand. Now why would I feel the need to put forth such an effort?

Stories of success not only give us hope, hope that difficult situations can be overcome, and point to paths that may be worth traveling. And in the case of Crohn’s and ulcerative colitis, two diseases that have claimed millions of victims and are exceptionally difficult to defeat, we need all the weapons we can add to our arsenal to achieve victory, one individual at a time. And, as you will soon discover, there are many weapons available from which to choose.

As we explore the options, I will look for opportunities to teach you valuable lessons about the disease you have, whether it be Crohn’s or ulcerative colitis, and I’ll start with the gray box that follows. And I promise, I won’t overwhelm you. Here, I will teach you the easy stuff. And all the while, I will try to entertain you a little, so you don’t fall asleep. You can thank me later.

I sense your eagerness to get right to it, so I will end the beginning with this:

While case reports are assigned limited level of evidence and are unable to deliver quantitative data, they still provide practical clinical real-world facts and are still indispensable for broadening medical knowledge. They provide an in-depth understanding of each individual case as opposed to large research studies with their “nomothetic approach.” Indeed, a case report is the only way to describe in details any unusual observations regarding symptoms, medical history, clinical findings, course of disease, pharmacological and non-pharmacological interventions and their complications, associations of diseases, side effects of drugs, etc. Consequently, a case report is a major educational tool that can inform readers on new observations, generate hypotheses, and facilitate detection of similar or identical cases. (Scarallo et al., 2021)

In essence

Both ulcerative colitis and Crohn’s disease are characterized by the disruption of the epithelial cell barrier and the dysfunction of the immune system. Disruption of the intestinal epithelial barrier in IBD allows the invasion of commensal bacteria. This leads to influx of inflammatory cells and their constant activation. ~Kristek and Loscher, 2014, emphasis added

While everything IBD is so complex, it is not all that difficult to understand what is basically going on. And it might be helpful to be in the know. So, here you go!

In the past, we were told that Crohn‘s and ulcerative colitis were autoimmune diseases. You can promptly dismiss this notion. Neither one is an autoimmune disease. They are something else.

More recently, and in the present, Crohn‘s disease and ulcerative colitis are characterized as diseases caused by a disordered (aberrant) reaction by the immune system to normal intestinal bacteria. While this theory may answer some questions, and undoubtedly aberrancy against intestinal bacteria does occur in both diseases, there is something clearly more fundamental in play that would answer the question,

“What is it that I have?” Here, I’ll do my best to explain.

In Crohn’s disease, the immune system has a serious problem dealing with bacteria that have arrived within the tissues and cells of the gut. Normally, this should not occur to any relevant degree, other than minor incursions that are quickly resolved. But due to genetic defects or unfavorable circumstances, the immune cells are unable to properly defend against and clear invasive bacteria, making Crohn’s an immunodeficiency disease which allows bacteria to persist within tissues and inside of cells. In support,

The notion that Crohn’s disease occurs as an aberrant reaction to commensal (typically present) microbiota in genetically susceptible hosts is widely regarded by physicians as fact. Yet although it is undisputed that Crohn’s disease is immune-mediated, an aberrant reaction to one’s own native flora is far from proven. (Campbell et al., 2012)

A substantial body of data has emerged in recent years to suggest that the primary defect in Crohn’s disease is actually one of relative immunodeficiency. (Marks et al., 2010)

And in Crohn’s, an immune cell called the macrophage is particularly defective in its role of clearing bacteria that have breached the layers of defense.

Recent work provides evidence of a failure of acute inflammation in Crohn’s disease (CD), and suggests that the primary defect operates at the level of the macrophage and cytokine release.

CD (Crohn’s disease) is a complex disease comprising multiple stages and phenotypes. We recently demonstrated that CD patients clear bacteria less rapidly than control individuals, which was associated with delayed recruitment of neutrophils and defective macrophage function. (Sewell et al., 2012, emphasis added)

When macrophages in the inflamed intestine show an enhanced pro-inflammatory phenotype, their ability to eradicate intracellular pathogens is decreased as their phagocytosis is significantly reduced. This probably accounts for recurrent infection in IBD Patients with pathogens that target macrophages, such as Mycobacterium paratuberculosis. (Kristek and Loscher, 2014, emphasis added)

Compared with Crohn’s, ulcerative colitis is less complex at its core. Ulcerative colitis occurs as the result of an immune response to bacteria that have breached the mucus layer of defense and colonize the surface of the rectum, and then colonize onward and upward to involve the colon, perhaps the entire colon.

Normally, luminal bacteria in the gut are withheld from contact with the epithelium by an adherent mucus layer, but in UC the bacteria reside on the luminal surface where they probably induce and maintain the inflammatory process. (Schneider et al., 2010, emphasis added)

Once damaged, the barrier is unable to exclude highly immunogenic fecal bacterial antigens [immune stimulating bacterial components] from invading the normally sterile submucosa. (Pravda, 2005)

In ulcerative colitis, it becomes obvious as to why all the inflammation is occurring. Bacteria are living where they should not be, and an ongoing immune response is necessary . . . and things spiral out of control.

I thought you would benefit from knowing my views on the fundamental nature of both Crohn’s and ulcerative colitis. But regardless of the fundamental cause, I clearly recognize that inflammation begets inflammation. So, efforts to control inflammation, be it with drugs or by other treatment modalities, can help turn things around and head the patient in the right direction, regardless of a specific cause.

I will conclude with this:

Although loss of tolerance to the gut microbiota [microbes] is demonstrated in animal models of inflammatory bowel disease, there is only limited evidence for this finding in patients with

Crohn’s disease and none in those with ulcerative colitis. (Danese and Fiocchi, 2011, emphasis added)

 

Clues

There are a few laboratory tests that you will find mentioned from time to time in the book. And since you are eager to learn, I will summarize the three most common ones here.

A CRP is a test that measures the concentration in the blood of a molecule called C-reactive protein, a molecule normally released during inflammation. Elevated values suggest the degree of disease severity. The higher the number, the greater the disease activity.

An ESR is a test that measures, in a standardized way, how fast red blood cells fall and settle at the bottom of a laboratory tube. Because inflammation promotes red blood cell clumping, and clumps of red blood cells fall faster than non-clumped red blood cells, an estimate of the degree of inflammation can be obtained. In this test, an abnormally high value indicates an inflammatory process is occurring somewhere in the body.

Finally, a Fecal Calprotectin is a test that measures the amount of calprotectin accumulating within the stool. Calprotectin is a molecule involved in the mobilization of a white blood cell type, the neutrophil, to sites of inflammation. An elevated fecal calprotectin level suggests intestinal inflammation is occurring, with a higher level inferring a higher degree of inflammation.

 

Basic terms and concepts

To better understand what is being said, there are a few terms and concepts that you will need to become familiar with as we continue.

The most relevant are:

Inflammation—a cell or tissue response to a threat such as injury or bacterial invasion, and is generally characterized by redness, pain, and swelling. It involves changes in metabolism and cellular behavior, as well as the production of specific molecules (complex proteins called cytokines) used to orchestrate the inflammatory response, a response that should defeat the enemy and lead to resolution (healing).

Cytokine—a regulatory protein produced by a cell for the purpose of promoting or decreasing an inflammatory response or influencing other cellular activity. For example, TNF-α and IL-10 are cytokines that act to increase the inflammatory response or decrease the inflammatory response, respectively. A cytokine produced by one cell may act locally, regionally, systemically, or even act on the cell of origin.

Inflammatory pathway—a series of cellular mechanisms that coordinate with each other to initiate and sustain a particular aspect of the inflammatory response. The inflammatory response is highly regulated. This requires cellular mechanisms that both activate or restrain a particular series of events that will increase

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