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Alyssa Luck

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Is the Low-FODMAP Diet Effective for IBD?

Alyssa Luck · Mar 14, 2022 · Leave a Comment

Summary: A low-FODMAP diet, which is a common intervention for IBS, is being increasingly studied in IBD patients. Unfortunately, the diet does not currently show efficacy for reducing inflammation, but has been shown in clinical trials to be effective at managing functional gastrointestinal symptoms in patients whose disease is in remission. Although a common concern with low-FODMAP diets is potential adverse effects on the microbiome from removing fermentable substrates, its actual effects on the microbiome in practice have not yet been clearly characterized, with inconsistent results across studies. For those who wish to support their microbiome on a low-FODMAP diet, resistant starch and Sunfiber are good low-FODMAP prebiotic options.

This article is part of the IBD Index. Last updated on April 20, 2022.

The low-FODMAP diet is somewhat unique among IBD interventions because it promises to intervene in the common but oft-overlooked situation of continuing functional gastrointestinal symptoms even in the absence of inflammation.

I cover the basics and practical aspects of a low-FODMAP diet in The Low-FODMAP Diet for IBD: Everything You Need to Know. In this article, I take a deep dive into all the evidence regarding the effectiveness of a low-FODMAP diet for IBD, both from the perspective of reducing inflammation and managing symptoms. I also address the most common concern about a low-FODMAP diet: its effects on the microbiome.

Table of Contents
Some context: IBS vs. IBD, and “functional” symptoms
Does a low-FODMAP diet reduce inflammation in IBD?
Interlude: not all FODMAPs are created equal
Is a low-FODMAP diet harmful to the microbiome?
Interlude: low-FODMAP does not mean low-prebiotic
Does a low-FODMAP diet reduce symptoms in IBD?

Some Context: IBS vs. IBD, and “Functional” Symptoms

Right off the bat, it’s important to clarify that the low-FODMAP diet is historically a diet for IBS, not IBD. Although the first appearance of the term “FODMAP” was in Peter Gibson’s 2005 paper about susceptibility to Crohn’s disease, it quickly became primarily a means to treat functional gastrointestinal symptoms (like the diarrhea, gas, bloating, etc experienced by IBS patients) that aren’t associated with intestinal inflammation (found in Crohn’s and UC patients).

Now, IBD patients do often present with functional GI symptoms that cannot be attributed to intestinal inflammation. In fact, about one quarter to one third of IBD patients who are in remission still experience significant functional GI symptoms. (Source 1, 2, 3, 4, 5)

Researcher Alexander Ford gives a good high-level summary of IBS vs. IBD here, and shares that even in 2020 when this paper was published, there existed no evidence-based standard of care for IBD patients with ongoing “IBS-like” symptoms; this is likely still true today.

That said, a 2018 clinical practice update (with none other than our friend Peter Gibson as a contributor) suggests a low-FODMAP diet as “best-practice advice” to address functional symptoms after inflammation, structural abnormalities, and alternative pathophysiologic mechanisms have been ruled out. There’s also some very exciting research coming down the pipeline (see the “coming soon” papers here).

All that said, there are two main angles from which the low-FODMAP diet should be assessed for IBD:

1. Effect on disease activity as measured by inflammatory markers and/or histological observation. This may or may not correlate with overall GI symptoms, but is still highly relevant (since the number one goal of IBD treatment is to quell inflammation).

2. Effect on overall GI symptoms (including “functional” symptoms). Essentially, the patient’s day-to-day experience of diarrhea, gas, bloating, constipation, urgency, etc.

I’ll discuss both of these below. I’ll also cover a third angle:

3. Effect on the gut microbiota. The effect of a low-FODMAP diet on the gut microbiota is related to both symptomatic and disease effects in IBD, and is likely a prime explanatory factor mediating these.

Does a Low-FODMAP Diet Reduce Inflammation in IBD?

As I’ve already hinted at, the low-FODMAP diet is not an intervention for IBD inflammation. That’s not what it was designed for, and as yet, there are no obvious direct mechanisms to implicate FODMAPs in the underlying disease pathology of IBD. And with a few minor exceptions, inflammation in IBD does not respond to FODMAP restriction in the clinical trials conducted thus far.

A 2020 review article by Grammatikopoulou et al points out that “most RCTs failed to include objective outcomes like immune activation markers, changes in the gut microbiota or in the gut lumen, and when objective outcomes (such as CRP, fCAL, or T-cell phenotype) were assessed, the lack of significant differences post-LFD adherence was apparent.” However, Bodini et al did observe a decrease in fecal calprotectin after a 6-week LFD trial in IBD patients. (Source)

Section 7 of this 2020 review article from Gibson does a good job summarizing all the research – both animal and human, and not necessarily IBD-specific – relevant to the effect of FODMAPs on intestinal injury and inflammation. As far as human research, one RCT in IBS patients found that a LFD led to reduced levels of urine histamine, which could suggest reduced immune activation. (Source)

A very small study in 6 IBS patients found higher levels of fecal LPS in the IBS patients compared with controls, but after 4 weeks of a LFD their LPS levels had decreased to a level similar to that of the healthy controls. (Source)

Another study, also in IBS patients, found that a LFD led to reduced levels of circulating inflammatory cytokines. (Source) This reduction of inflammatory cytokines was accompanied by a reduction in certain intestinal bacteria believed to be beneficial, and interestingly, a period of supplementation with fructooligosaccharides (a FODMAP) restored levels of those bacteria without increasing levels of cytokines.

The remaining findings he discusses (which I won’t summarize here) begin to implicate FODMAPs in more serious intestinal barrier dysfunction, injury, and inflammation, but this data is from animal studies that have tenuous relevance to humans at best. Not only are the doses of FODMAPs used in these animals quite high, but the diets are so deconstructed they can scarcely be called food. And as I’ll explain below, the effects of FODMAPs can be quite dependent on context, with whole-food FODMAPs having notably different effects from isolated supplemental FODMAPs.

That said, Gibson has not abandoned his hypothesis that excessive intake of FODMAPs could contribute to the development of IBD (see Section 8 of the previously mentioned review article), so it’s certainly still an open question in the research community. But at this time, there isn’t much support for the use of a LFD as an intervention for IBD inflammation.

Interlude: Not all FODMAPs are Created Equal

In his 2005 “personal view,” Gibson presents a rat study showing that supplementation with rapidly-fermented fibers caused significant intestinal injury. He mentions this study again in his 2020 review paper, but presents no new evidence to that effect. Based on this and other tangentially-related animal evidence, he suggests that FODMAPs could potentially cause intestinal injury by virtue of their rapid fermentation in the distal small intestine and proximal colon.

First of all, although FODMAPs are indeed rapidly-fermented by definition, this rat study did not use a FODMAP in the experiment – it used potato starch (a source of resistant starch). But more importantly, the harmful effects were reduced or abolished by the concomitant supplementation of wheat bran, a slow-fermenting fiber. It appears that consuming slow-fermenting fibers along with rapidly-fermented fibers shifts fermentation towards the distal end of the colon, which our intestines seem to prefer over excessive fermentation in the proximal colon and ileum.

This topic could be explored in far more depth, but I take this as yet more evidence that there’s something to be said for eating foods in their whole form, since most FODMAP-containing foods include many different types of fiber, including the slowly-fermenting kind.

Is a Low-FODMAP Diet Harmful to the Microbiome?

The same Gibson 2020 review paper I extensively referenced in the last section also does a good job summarizing what we know about the effect of a LFD on the intestinal microbiota, which is…not much.

Based on the evidence so far, we can surmise with some certainty that a LFD leads to decreased abundance of microbes in feces (without associated decrease in richness/diversity), and decreased abundance of the phylum Actinobacter and genus Bifidobacterium, but all other effects on the microbiota seem to be inconsistent and unpredictable, owing in large part due to the huge number of variables that aren’t strictly controlled for across studies: specific composition of the LFD, FODMAP content of subjects’ habitual diet, differential effects of different types of FODMAPs in the diet, etc. (Additional source for review of the evidence)

And any useful interpretation of these results is further complicated by the fact that despite claims and appearances, we don’t actually know what constitutes a “healthy microbiome.” (This fact alone shows how much we still have to learn in the field of microbiome science, but for now it should at least release us from the cognitive dissonance when confronted with symptom reductions that correlate with “unfavorable” microbiome shifts, for instance.)

As far as the effects on SCFA, one would expect that a LFD would lead to reduced SCFA production, since bacteria would have less fermentable substrate. That may well be true in many cases, but most of our human data is from SCFA measurements taken from feces, and since SCFA are readily absorbed from the intestine, the SCFA that show up in feces were probably produced by bacterial fermentation of long-chain fibers (non-starch polysaccharides and resistant starch) rather than FODMAPs.

This inference is supported by the fact that studies that matched fiber content between LFD and control diets (usually by adding resistant starch to the LFD) showed no difference in fecal SCFA, while those that did show a difference did not match fiber content.

Much of the discussion on the effect of a LFD on gut microbiota gets into real can-of-worms territory by calling up what I see as one of the Big Central Questions of Intestinal Health and Disease (or BCQIHD…think it’ll catch on?), namely: starve the bad or feed the good?

This question, referred to in at least one article as “Gibson’s Conundrum,” is at the mechanistic intersection of therapeutic diets such as the Specific Carbohydrate Diet, low-FODMAP diet, and even carnivore or ketogenic diets, and therapeutic approaches emphasizing increased consumption of prebiotic fibers (whether through diet or supplements) like the bean protocol.

Tackling that question is very much outside the scope of this article, and a satisfying synthesis of the dual hypotheses depicted below continues to elude even cutting-edge researchers, so I’d certainly fare no better. Suffice it to say that a low-FODMAP diet most certainly affects the intestinal microbiome, in ways that may have bearing on IBD pathology, but as yet we don’t have a consistent picture of what those effects are or whether they’re helpful or harmful or some combination of the two.

Caption from source: “Alternative effects of elevated FODMAP intake: A, Higher FODMAP intake might have prebiotic effects with associated health benefits. While increasing the relative abundance of Bifidobacteria is well-documented, supportive human data for health benefits are limited. B, Higher FODMAP intake might pathogenically contribute to IBS. Based largely on animal studies with limited human supportive data, higher daily FODMAP oligosaccharide intake may lead to reversible mucosal injury. Repeated intakes above this critical level will cause repeated insults and lead to changes in the enteric nervous system manifesting as elevated visceral sensitivity”

Interlude: Low-FODMAP Does Not Mean Low-Prebiotic

Gibson introduces this issue clearly and succinctly: “FODMAPs are defined by their molecular size, absorptive characteristics in the small intestine, and fermentability. Prebiotics are defined by their effects on microbiota and health, and are substrates that are selectively utilized by host microorganisms conferring a health benefit.” (Source)

He goes on to explain that many dietary carbohydrates that have prebiotic actions are FODMAPs, including FOS, GOS, polyols, and possibly fructose. I would also add “possibly lactose” to that list. (Source 1, 2, 3)

But although many FODMAPs are prebiotics, not all prebiotics are FODMAPs. Resistant starch is probably the best example of a fiber that is commonly considered a prebiotic, but is not a FODMAP. In fact, in LFD trials where fiber content is matched between the experimental LFD and the control diet, resistant starch is typically added to the LFD to make up for the reduction in fiber content from high-FODMAP sources. (Sunfiber is another low-FODMAP prebiotic option.)

So setting aside the question of whether and how and to what extent prebiotics are necessary or beneficial for managing IBD (or for maintaining the health of the microbiome in general)…I want to at least make the point that the categories “FODMAP” and “prebiotic” are not one and the same, and that there are low-FODMAP options for selectively encouraging the growth of “beneficial” bacteria for those who desire to do so.

Does a Low-FODMAP Diet Reduce Symptoms in IBD?

And finally, we reach the main event. In contrast to its effects on intestinal inflammation and the microbiome, the effects of a LFD on functional GI symptoms (both in people with IBD and IBS) are fairly well established, so this is where a low-FODMAP diet really comes into its own: in IBD patients who have ongoing functional symptoms that are not explained by inflammation.

The controlled trials by Cox et al (2020), Bodini et al (2019), and Pedersen et al (2017) provide evidence that initiating a LFD can improve symptoms and quality of life for patients with quiescent IBD, while results from the trials by Cox et al (2017) and Halmos et al (2016) provide evidence for the flip side of the same coin – that increasing FODMAP intake in IBD patients leads to worsened symptoms. (See the review of the literature section in my other low-FODMAP article for additional details on all these studies, plus other relevant papers.)

The mechanisms by which FODMAPs contribute to functional GI symptoms are also fairly well understood, lending credence to the causal relationship. As explained here, what makes a FODMAP a FODMAP is both 1) its molecular structure/size as a short-chain carbohydrate, and 2) its tendency to be poorly absorbed and readily fermentable by bacteria.

Based on these characteristics and confirmed by ileostomy study, breath testing, and other techniques, researchers have confirmed that FODMAPs can lead to GI symptoms via 1) osmotic effects, resulting in more water being drawn into the intestine, and 2) increased gas production from bacterial fermentation. (Source)

Although this is a bit out of scope for this article, it’s important to note here that an inevitable causal linkage need not be drawn from FODMAPs > increased gas > GI symptoms. In reality, the relationship is much more complex, with factors such as composition of gut bacteria, visceral hypersensitivity, and gas disposal mechanisms also at play. After all, plenty of healthy people can consume quantities of FODMAPs without issue.

The Bottom Line

  • Some very preliminary evidence indicates that a low-FODMAP diet could help reduce inflammation, but it is far from being a validated strategy for that purpose.
  • On the other hand, we have fairly good evidence that low-FODMAP diets are effective for reducing lingering functional gastrointestinal symptoms in IBD patients whose disease is in remission.
  • Although a common concern with low-FODMAP diets is potential adverse effects on the microbiome from removing fermentable substrates, its actual effects on the microbiome are not clear and predictable on the basis of current research.
  • Not all prebiotics are FODMAPs, so it’s possible to support the growth of beneficial bacteria through resistant starch or products like Sunfiber even on a low-FODMAP diet.

Related

Deep Dives, Therapeutic Diets for IBD carbohydrates, Crohn's disease, fiber, fodmap, gut bacteria, IBD, low-FODMAP, microbiome, prebiotics, ulcerative colitis

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Hi! I’m Alyssa. I like thunderstorms and cats, hate wearing shoes, and enjoy devising extensive research projects for myself in my free time. This is me in Bali with a monkey on my shoulder. And this is my blog, where I muse about health-related topics and document my relentless self-guinea pigging. If you want to know more about me, click here!

alyssa.luck

alyssa.luck
If you've seen "vagus nerve exercises" that have y If you've seen "vagus nerve exercises" that have you moving your eyes or tilting your head, you've probably encountered the work of Stanley Rosenberg. The exercises he created and introduced in his 2017 book now appear in instructional videos all over the internet. 
 
The book itself has much to recommend it: it's accessible, it's practical, it's inspiring. But it has one major flaw: the solid practical and informational content regarding the cranial nerves is framed in terms of the scientifically dubious polyvagal theory. 
 
I particularly enjoyed the book as an introduction to the therapeutic arena of bodywork, of which Rosenberg is a skilled practitioner. His book is full of case reports that demonstrate how immensely powerful extremely subtle movements and physical manipulations can be. These do need to be kept in perspective: it's a small sample size of the most remarkable cases, and the results were achieved within the supportive clinical environment of a skilled practitioner. You can tell from his descriptions how refined his technique is. But nevertheless, it was a paradigm-shifting read for me, and the exercises give you something concrete to play around with. 
 
The book also brought the cranial nerves and the concept of “social engagement” to the fore as arbiters of health. Rosenberg has a solid background in cranial nerve anatomy and shares many interesting tidbits and considerations that you don’t typically hear; for instance, the potential impact of dental and orthodontic work on cranial nerve function.
 
So, is it worth reading? If any of the above piques your interest, go for it! Just read my post on polyvagal theory first – you can use the book to practice separating the wheat (solid informational content) from the chaff (pseudoscientific framing). If nothing else, the book is a nice reminder that genuine healers who get lasting results for their patients do exist.

But if you just want to try the exercises, you can easily find them all on YouTube. 

“You learn techniques to understand principles. When you understand the principles, you will create your own techniques.” -Stanley Rosenberg
I first stumbled upon polyvagal theory during the I first stumbled upon polyvagal theory during the course of my heart rate variability research. I was surprised to encounter it again "in the wild" shortly after, in the book "Accessing the Healing Power of the Vagus Nerve." Before long, I saw it popping up everywhere, (Baader-Meinhof, anyone?) 
 
Digging deeper, I discovered scientific controversy bubbling just beneath the smooth surface of polyvagal theory's popular presentation. Three months later, I posted a 13k word analysis of the topic. 
 
The technical details are far below the level of practicality for the average person, but the way polyvagal theory has propagated outside of academia has some important ramifications for clinical and scientific progress. 
 
In the wake of a wave of health complaints that our current medical model is poorly equipped to treat, it's clearer than ever that a new paradigm is needed. The grassroots push to emphasize diet and lifestyle factors has been a huge step in the right direction, but it's becoming more and more common to see people who have done everything "right" and are still struggling with persistent health complaints that could range anywhere from mildly annoying to debilitating. 
 
What we need is a genuine integration of mind and body in medicine – not the weak lip service that our current paradigm pays to "stress reduction," like the vague suggestion to relax more and maybe try meditation. And if we're going to develop a sophisticated mind-body medicine, we need a sophisticated mind-body science. And if we want a sophisticated mind-body science, we must subject such topics to the same standards of inquiry as we expect from molecular biomedicine. And that means rejecting pseudoscience like polyvagal theory. 
 
Full analysis and references at alyssaluck.com/polyvagal-theory-a-critical-appraisal
To continue my recounting of the health things I'm To continue my recounting of the health things I'm experimenting with, let me tell you about DNRS: the slightly cheesy, arguably outdated “brain rewiring” program that has changed my life. 

I found it because I was looking for ways to “retrain” my nervous system. I watched some success stories. None of the “target” health conditions matched mine, but I went for it anyway. Probably the best decision I’ve ever made for my health. 

The core of DNRS is built on the principles of neuroplasticity. They call it "brain rewiring" because you intentionally take triggers that would normally stimulate a negative response in your body or mind, and associate them repeatedly with neural signals of safety. If that sounds pseudosciencey, I hear ya – one of my goals with future posts is to bring some concreteness and specificity to the topic. I imagine there are lots of people who could benefit from this type of thing who are turned off by the overly abstract or touchy-feely language. 

There are tons of "brain rewiring" programs like DNRS, but they're all built on similar ideas. Most bring in elements of other popular approaches, ranging from the scientifically validated (cognitive behavioral therapy, mindfulness, acceptance and commitment therapy) to the type of new-agey stuff I always scoffed at (shadow work, inner child work, parts work). 

For me, DNRS has provided the perfect framework to finally achieve what meditation experts and therapists and mystics alike are always advocating – the ability to step into the role of “curious observer.” It's given me everything therapy and meditation promised but could never deliver, helping me recognize my own patterns of thought and behavior and consciously redirect unhelpful ones. If this sounds vague, that's because there isn't a single area of my life that hasn't been improved by using this framework. 

I spend far more time in states of joy and peace and gratitude, and less time in states of anxiety or depression or frenzy. Many chronic worries that used to occupy my mind or keep me up at night – whether related to health, relationships, or my future – have disappeared, and the others are on their way out. (Cont. in comments)
Isn’t it crazy how something can be so easy and Isn’t it crazy how something can be so easy and natural for one person, but so hard for another? 

Me doing food: I can totally cook everything I eat from scratch, no prob

Me doing mental health: just doing my hour of daily mindful cognitive gratitudinal journalization

Me doing physical therapy: I can’t do it I don’t have that muscle

I’ve done many hard things in the name of health, but I think they’ve all been the types of hard things that come naturally to me. And frankly, that hasn’t gotten me where I want to be. 

So I’ve decided to finally tackle something that feels very unnatural: developing a real relationship with my muscles and bones, and learning - through experience, not from a book - how they coordinate with each other and how to use them. 

I never really considered my musculoskeletal system a key player in autoimmune or digestive woes, but now I realize it’s naïve to think dysfunction in one part of the body doesn’t affect another. And since this is so obviously my weakest link, it’s high time to make it a priority!

Even though I’ve done strength training in the past, I never dedicated the time and focus to figure out what my body actually needed to function better, and workouts often felt awkward or led to injury. 

I’ve always dreaded PT-type exercises because they felt simultaneously like “not enough” and also SO HARD, especially when there’s no way to confirm whether I’m doing them “right” (my nightmare). 

But I’m pretty sure the fact that targeted “mind-muscle” work is so hard for me means it’s what I need the most. (That’s how that works, right?)

Anyway, I’m happy to report that I’m finally through both the initial phase of being a giant baby because I have to do something I’m bad at, AND the second phase of neurotically worrying about doing it “wrong.” And hopefully I’m on my way to better posture, improved breathing, and greater strength! 

Super thankful to have people in my life who remind me to have fun and stay curious, when my natural disposition is to write a 27-step plan to “fixing” everything “wrong” with me. And to remind me that it is, in fact, a JOY to be a novice at something (as @_john_the_savage_ would say).
"If your nervous system is balanced, your heart is "If your nervous system is balanced, your heart is constantly being told to beat slower by your parasympathetic system, and beat faster by your sympathetic system. This causes a fluctuation in your heart rate: HRV." (whoop.com) 
 
This statement is a formidable example of one of the biggest misconceptions about heart rate variability (HRV). 
 
HRV is highest during rest or sleep, when sympathetic input is lowest. If HRV was the result of an autonomic “tug-of-war,” why would it be greatest when one of the contenders has entirely dropped the rope? 
 
Part of the misunderstanding may stem from failure to recognize that the heart has an intrinsic rate, well above the resting heart rate maintained by the vagus nerve. Varying vagal impulses create HRV without any sympathetic input at all. 
 
There are many other common misconceptions, such as the notion that HRV metrics measure autonomic tone, or that HRV itself is a metric with one interpretation. 
 
Such misconceptions aren’t only found in layscience – they also pervade academic and clinical literature. For instance, you’ll see LF used as a measurement of “sympathetic tone” and LF/HF as a measurement of “sympathovagal balance,” even though it’s been clear for decades that those interpretations are not physiologically accurate.
 
This post (and the associated article at alyssaluck.com/hrv101) can be thought of as “foundations for understanding HRV research.” And it provides a good example not only of the insufficiency of “sound-byte” science, but also of real science in action. 
 
The unfortunate reality is that we can’t always take researchers’ conclusions at face value. Few have the time to adequately assess a field before adopting one of their metrics, and once a misinterpretation has taken root it can easily become an accepted fact that propagates through repetition, becoming more entrenched with each published paper.
 
Thankfully the ramifications in this case are not very serious - misdirection of experimental design and analysis, and many false statements, but no dire consequences. Nevertheless, it’s a good reminder that science is a human institution, and it never hurts to question oft-repeated “facts.”
My latest diet experiment: the bean protocol! This My latest diet experiment: the bean protocol! This was one of the changes I made immediately prior to my drastic increase in HRV. 

Brief background: the bean protocol entails eating lots of soluble fiber (particularly beans) as a way to support detox. It rests on the assumption that most chronic health issues are the result of fat-soluble environmental toxins, excess hormones, and other fat-soluble things being recirculated in the body rather than eliminated. 

There is some scientific merit to this: the liver does eliminate many toxins and other compounds through the bile, these things can be subject to reabsorption via enterohepatic recirculation, and certain types of fibers do interrupt this process by binding bile, preventing reabsorption and allowing excretion in the feces.

That said, there are many unanswered questions that would need to be answered for me to be on board with that as the sole or even primary explanation for the anecdotal success of those on the protocol. I think there are almost certainly other mechanisms at play, and I doubt things work exactly as proponents of the protocol describe. 

But at the end of the day, what matters is not mechanisms, but practical outcome. And whatever the reason, it works for many! It seems especially popular and effective for hormonal issues and acne, but the preeminent bean spokesperson @uniquehammond cured her severe Crohn’s with it. 

For me, I experienced better digestion and clearer skin, among other benefits (like not having to wear deodorant). On the less-good side, I lost weight I didn't need to lose, had cold hands and feet, and developed some dry patches on my skin. 

(The dry patches [and perhaps weight loss] were probably because I kept fat too low – mostly because their favored fat source, nuts, is a no-go for me.)

I'm continuing to experiment, hoping to find a balance that lets me reclaim the benefits (which I lost after returning to my normal eating pattern) while avoiding the pitfalls. I’ll share any exciting developments, and will eventually dig into the science behind it too. 

For info about what the protocol entails, you can visit alyssaluck.com/the-bean-protocol-for-ibd!
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