Unfermented β-fructan Fibers Fuel Inflammation in Select Inflammatory Bowel Disease Patients

[kiny]

https://www.gastrojournal.org/article/S0016-5085(22)01150-7/fulltext

Unfermented β-fructan Fibers Fuel Inflammation in Select Inflammatory Bowel Disease Patients


Background & aims
Inflammatory bowel diseases (IBD) are affected by dietary factors, including nondigestible carbohydrates (fibers), which are fermented by colonic microbes. Fibers are overall beneficial, but not all fibers are alike, and some patients with IBD report intolerance to fiber consumption. Given reproducible evidence of reduced fiber-fermenting microbes in patients with IBD, we hypothesized that fibers remain intact in select patients with reduced fiber-fermenting microbes and can then bind host cell receptors, subsequently promoting gut inflammation.

Methods
Colonic biopsies cultured ex vivo and cell lines in vitro were incubated with oligofructose (5 g/L), or fermentation supernatants (24-hour anaerobic fermentation) and immune responses (cytokine secretion [enzyme-linked immunosorbent assay/meso scale discovery] and expression [quantitative polymerase chain reaction]) were assessed. Influence of microbiota in mediating host response was examined and taxonomic classification of microbiota was conducted with Kraken2 and metabolic profiling by HUMAnN2, using R software.

Results
Unfermented dietary β-fructan fibers induced proinflammatory cytokines in a subset of IBD intestinal biopsies cultured ex vivo, and immune cells (including peripheral blood mononuclear cells). Results were validated in an adult IBD randomized controlled trial examining β-fructan supplementation. The proinflammatory response to intact β-fructan required activation of the NLRP3 and TLR2 pathways. Fermentation of β-fructans by human gut whole microbiota cultures reduced the proinflammatory response, but only when microbes were collected from patients without IBD or patients with inactive IBD. Fiber-induced immune responses correlated with microbe functions, luminal metabolites, and dietary fiber avoidance.

Conclusion
Although fibers are typically beneficial in individuals with normal microbial fermentative potential, some dietary fibers have detrimental effects in select patients with active IBD who lack fermentative microbe activities.

 

[kiny]

Stay clear from the "feed the good bacteria" and "probiotic" folks. We have plenty of data that these bacteria and the fodmap they use as fuel are involved in inflammation. The most effective diet for crohn's disease is EN that lacks fermentable fiber. If you are eating fibers, know what you're eating. Not all fibers are created equal. The amount of glucans, fructans, lignin and cellulose all differ. There are many studies out there that will tell you which foods contain which types of fiber.

 

[patulsius]

@kiny Is there a list with those foods that mostly contain b-fructan fibers? I know a few of them like chicory root, asparagus or garlic, but I would like to know all of them just to make sure I do not include them on my diet.

By the way, anyone knows if bananas are also high on b-fructans, because they are traditionally considered a safe food for Crohn and it is also very used on the SCD protocol, even for the intro diet wich is the safest diet available according to SCD.

 

[kiny]

It is easy to find FODMAP content for fruits and vegetables, it is more difficult for grains because it depends on the processing.

I think to make any list manageable you should ask yourself why you want to consume fiber. You can get all nutrients you need in a diet, and avoid consuming any fermentable fiber, as EN and low-FODMAP diets have shown. There's a lot of hoopla about SCFAs, butyrate, feeding the microbiome, etc, but plenty of carnivores do not consume fermentable fiber and they do more than fine without them. "you need to feed the microbiome" is 21st century baloney. The number of people suffering from SIBO, IBS, and fructose intolerance, etc, is staggering. SIBO and fructose intolerance are both linked to crohn's disease.

Nevertheless, certain specific fibers do have an interesting function, and that is as a bulking agent that can relieve constipation. The outer cell wall of plants contain cellulose that is a great bulking agent.

But you need to be selective if you want to avoid fructans. The bran of Rye might structurally contain cellulose, but Rye also has high amounts of fructans, higher than many other grains. If you want to avoid fructans, you should avoid rye. It depends on the grain and how it is prepared. Which grain is it, is it bran or not, etc. All the data is there if you look for it.

 

[kiny]

https://academic.oup.com/ecco-jcc/article/11/12/1420/3835798?login=false

Fermentable Carbohydrates [FODMAPs] Exacerbate Functional Gastrointestinal Symptoms in Patients With Inflammatory Bowel Disease: A Randomised, Double-blind, Placebo-controlled, Cross-over, Re-challenge Trial

Background and aims: Preliminary evidence suggests that fermentable carbohydrate restriction might ameliorate functional gastrointestinal symptoms [FGS] in inflammatory bowel disease [IBD]. Our aim was to determine whether fermentable carbohydrates exacerbate FGS in IBD using a randomised, double-blinded, placebo-controlled, re-challenge trial.

Methods: Patients with quiescent IBD and FGS responsive to a low FODMAP diet were allocated to a series of 3-day [d] fermentable carbohydrate challenges in random order [fructan, 12 g/d; galacto-oligosaccharides [GOS] 6 g/d; sorbitol, 6 g/d; and glucose placebo, 12 g/d], each separated by a washout period. Symptoms and stool output were measured daily during the challenges.

Results: Thirty-two patients with IBD, fulfilling criteria for irritable bowel syndrome, functional bloating, or functional diarrhoea, were recruited and data were available for 29 patients completing all arms [12 Crohn's disease, 17 ulcerative colitis]. Significantly fewer patients reported adequate relief of FGS on the final day day of the fructan challenge [18/29, 62.1%] compared with glucose [26/29, 89.7%] [p = 0.033]. There was greater severity of pain [1.1 vs 0.5, p = 0.004], bloating [1.3 vs 0.6, p = 0.002], flatulence [1.5 vs 0.7, p = 0.004], and faecal urgency [0.9 vs 0.4, p = 0.014] on the final day of fructan challenge compared with glucose.

Conclusions: At the relatively high doses used, fructans, but not GOS or sorbitol, exacerbated FGS in quiescent IBD. Further research is required to determine whether a low FODMAP diet reduces FGS in IBD and the degree of FODMAP restriction required for symptom improvement.

 

[kiny]

Up until a few years ago, the main recommendation for crohn's diease patients were low fiber diets, low residue diets, bowel rest and elemental nutrition. This is based on scientific evidence, the amelioration of disease activity in people on EN which lack any fiber, the benefits of enteral feeding and the benefits of low residue diets. The fact bacteria involved in crohn's disease like Klebsiella ferment large amounts of starches. The fact people with crohn's disease often have SIBO. The fact fecal matter is linked to inflammation in crohn's disease (Rutgeerts, Harper). The fact there are anti-saccharomyces cerevisiae antibodies in crohn's disease.

This idea that people with crohn's disease should consume fiber seems to be a very recent recommendation and there is no scientific basis for it. It seems largely based on a study that argued people who consumed diets rich in fiber had supposedly a lower chance of developing crohn's disease. This tells you nothing. You could just as easily build a case against fiber with this data and argue that people without intestinal issues naturally don't have a problem with fiber and consume more fiber because of it. Not does it tell you anything about people who actually have crohn's disease.

 

[kiny]

The fact these arguments of consuming fiber comes from the same group of people who advocated for fecal transplants in crohn's disease, until the trials had to be stopped after 2 days because people had CRP and calprotectin shoot through the roof, should make anyone wary. If a GI recommends fiber to a patient with crohn's disease, they better have a better reason for it than "help the good bugs".

 

[asadmom]

The fact these arguments of consuming fiber comes from the same group of people who advocated for fecal transplants in crohn's disease, until the trials had to be stopped after 2 days because people had CRP and calprotectin shoot through the roof, should make anyone wary. If a GI recommends fiber to a patient with crohn's disease, they better have a better reason for it than "help the good bugs".

Sorry... you mean the Armstrong Lab advocated the fecal transplants for CD?

 

[kiny]

No, they're not recommending fiber or prebiotics. I am saying that there's many researchers who put forward the idea that they could influence inflammation by modulating the microbiome. Fecal transplants, probiotics, prebiotics (inulin, fiber). These have all hurt patients, not helped them.

The probiotics trials failed, the prebiotics (fermentable fiber) trials failed, the fecal microbiome trials failed.

 

[kiny]

Many of these trials don't seem to want to learn. Every decade the same trials are done that make people with crohn's disease sick.

Rutgeerts and Harper showed that the fecal stream caused inflammation decades ago. A few years ago researchers ignored all this data, and did fecal stream experiments, causing inflammation in many patients.

We have tons of old studies where people were given prebiotics, fermentable fibers. They made most patients sick. But now you hear of GI arguing that people with crohn's disease should start consuming lots of fermentable fiber. No scientific basis for this. Dysbiosis they argue. Dysbiosis is a result of inflammation and resolves itself after inflammation subsides.

People with crohn's disease are not there to experiment on. Leave these people alone and make sure they get the treatment they need to lower inflammation. We know what works.

Bacterial load studies are interesting, how transit time influences this, how dietary factors influences this. But trying to manipulate the microbiome has cost billions, and got research nowhere.

 

[Ignotius]

i think i get part what you are saying......i dont take it to the same extreme tho.....it follows well enough logic to me, up to a point, but sometimes we also DO see the chicken did come first and it came from across the road.....etc etc lol....

i.e. they may have disregarded some "baddies" with EN studies and found some useful data there.....but i cant for the life of me say ok if im not flaring i can eat all this stuff thats been known to encourage bad bacterial growth, which CAUSES inflammation....it just does.....it will take alot to convince me otherwise......i think its actually one of the root causes once we consider this is a progressive disease....its a little indigestion and imbalance until its not...

i fully agree tho that most of these studies make me feel like have their heads up some dark place and/or arent trying and/or dont have the slightest clue to begin with.

i did find it sort of amazing tho like all these herbal and dietary whatever they found to "decrease inflammation", seems hopeful....just that it is more complicated than they can easily say even, not that i would dive to trusting such a simple solution like ok just eat more "blah blah" and its fine.

then things like the fiber stuff i really just think it matters like, what type, how easy they are broken down given the current condition of the disease and individual etc....or like prebiotics, i really dont think can be lumped in one category....or even 2 probably.....we have things like epicor working on several levels and prefermented....things like benefiber that idk why or how but it makes things better for me.....then you see these chewable things with artificial sugars etc like WTAF...counter the exact thing its meant to help because if it doesnt taste like candy im not taking it.....no wonder we got here so easy as a species...or others like the larch some ppl swear by but my body did not seem to like.....fruits yes, veggies no....millets, superfoods, select supplements.....idk, i got side tracked by this stage 3 kidney disease i guess some trainee told me i have because no doctor actually did....the whole system is a pretty bad eyeroll....from the making of these foods, to the healthcare system treating us for trusting them and eating them.

 

[lukesjr]

Interesting discussion. My GI recommended fiber to me. Psyllium husk has dramatically improved my condition. Benefiber seemed to make me feel worse.

 

[kiny]

i did find it sort of amazing tho like all these herbal and dietary whatever they found to "decrease inflammation", seems hopeful....just that it is more complicated than they can easily say even, not that i would dive to trusting such a simple solution like ok just eat more "blah blah" and its fine.

There are several experiments, which I do support, whereby inflammation is controlled by EN or anti-TNF, and the experiment tries to get people to a state where they remain in remission even when anti-TNF and EN are gradually reduced.

A Japanese team has claimed for several years now they can get people in remission with EN or anti-TNF and transition them to a diet where they remain in that state and don't relapse. This has been copied by experiments in the West.

The difference with dietary intervention studies is that the dietary intervention is not used to induce remission. It's used to prevent relapse. EN or anti-TNF are used to induce remission, the dietary change is there to get people onto a sustainable path whereby the patients remains in long-term remission.

 

[kiny]

What these teams are doing is not new either. When they started giving patients ani-TNF 25 years ago, it was never given every 8 weeks. It was given once and then dietary changes were used to try to keep people in remission.

Chronically giving people biologics is pretty new, and it usually results in therapy escalation because most people relapse on biologics within 1 year. So these patients are constantly switched from biologic to biologic until they run out of options. It's not a solution, there needs to be a path whereby you reduce these biologics and get them onto a sustainable path.

 

[kiny]

2012 comment on study where the addition of fructo-oligosaccharides was used as a prebiotic in crohn's disease patients.

Not only was the addition of fermentable fiber ineffective, a number of patients had to withdraw from the study due to worsening symptoms and abdominal pain.

Note that these studies, done around 2000-2010, were very well designed, and multiple studies showed similar results. The addition of prebiotics, inulin, was ineffective and worsened outcomes.

I would be very apprehensive of anyone suggesting people with crohn's disease should consume fiber/prebiotics on the basis of modulating the microbiome.

When Rutgeers and Harper filtered the fecal stream in the 80s with an ultrafiltrate, it removed large dietary particles and inflammation subsided. This would have filtered out bacteria and fungi, but also large fibrous dietary particles.

The one commonality between all these types of EN that result in remission, is their complete lack of fiber. EN were never originaly designed to treat crohn's disease. They were used for malnutrition, including in crohn's disease patients. By pure luck studies figured out it also lowered inflammation.

The lack of fiber in EN is simply because of its form, it's a powder, there are osmolality considerations. If EN works because it lacks fiber, it would be be a luck of the draw. But the fact EN completely lack fiber and are so effective in inducing remission, is very interesting.

 

[kiny]

When you think about EN and their original application in treating malnutrition and subsequent use in tube feeding, you are simply naturally drawn to making a product that lacks fiber.

If you design EN on the basis of treating malnutrition, you want a certain caloric density and osmolality. You are naturally drawn to something with small dietary particles that are readily absorbed. Glucose, MCT. You simply end up at these ingredients.

EN don't have fiber because they had to meet certain criteria, not because they were designed to treat crohn's. If, and that's a big if, EN are effective because they lack dietary fiber, it is a luck of the draw.

 

[kiny]

Some studies proposed that dietary fiber consumption is protective against the development of crohn's disease. Most of these are from the US.

I can not find a link between dietary fiber intake being protective against development of crohn's diseae outside the US, if anything low dietary fiber intake seems protective against the development of crohn's disease.

The EU uses large consumption surveys, similar to the US Survey of Food Intake from the 90s, to assess fiber intake.
https://knowledge4policy.ec.europa.eu/health-promotion-knowledge-gateway/dietary-fibre-overview-3_en

Norwegians had the highest survey reported fiber intake in Europe. Yet multiple studies show Norway has the highest incidence of crohn's disease in Europe and some of the highest in the world.

Another study showed Norwegians, Danes, Swedes, Germans and French had much higher dietary fiber intake than intake of mediterranean countries. Yet in Southern Europe, especially the iberian like Spain, where daily fiber was reported to be much lower, incidence of crohn's disease is much lower. The EU consumption survey supports the data that daily fiber intake is much lower in Iberia, yet incidence of crohn's disease in Spain and Portugal is also much lower.

In France there is a North-South gradient where the largest number of cases of crohn's disease are strictly found in the North. Dietary fiber intake was reported to be higher in Northern France.

Intake of dietary fiber in Japan was reported to be considerably lower than European countries, yet Japan has a very low incidence of crohn's disease among developed nations.




https://www.researchgate.net/public...endations_intakes_and_relationships_to_health

Argentina, with much lower dietary fiber intake than Austrialian 4-12 year olds, has a much lower incidence of crohn's disease.



https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8079254/

 

[kiny]

Adam Stein and Russel Cohen, University of Chicago Medicine, pointed out the dangers in some of these fiber studies.

The suggestion that people with crohn's disease should consume more fiber, is largely based on the fact that people without crohn's disease seem to eat more fiber and people in remission consume more fiber also.

These studies then conclude that low-fiber diets should be reconsidered and then, to my great alarm and some others, suggest people with crohn's disease should consume more fiber.




Adam Stein and Russel Cohen pointed out the dangers with these type of conclusions.

It would be dangerous to conclude that people with gluten intolerance should consume more gluten, based on the fact people without gluten intolerance consume gluten.

Just like it would be very dangerous concluding that people with lactose intolerance or food allergies, should consume lactose, based on the fact all the people without lactose intolerance consume lactose.

If fiber causes people with crohn's disease distress, it is only natural that they would stop eating fiber. And suggesting these people consume more fiber, is a very dangerous conclusion.

More studies are needed, but suggesting people with crohn's disease should consume more fiber because some in remission or some withouth crohn's disease consume fiber, is a very dangerous conclusion. It is just as likely, if not more likely, that people with crohn's disease, just like people with IBS, gluten intolerance and allergies, avoid certain dietary products, because it causes them issues.

The fact EN, which lack any fiber, have the highest known remission rates, puts those people advocating for more fiber intake, in a very difficult position.

 

[kiny]

If a Western high caloric diet of fats and refined carbohydrates, and a lack of fiber intake from fruits and vegetables, was behind the prevalence of crohn's disease, you would expect people with crohn's disease to suffer from other ailments linked to these diets. I can't speak for every country, but people in my country in Europe who develop crohn's diseaese are anything but obese, I think I was the thinnest person in my class and ate a diet low in fat and low in refined carbs.

EN, a highly processed dietary source, high in refined carbohydrates, relatively high in fat, and completely lacking any fiber, results in rapid remission.

 

[kiny]

A very strong environmental link, that is a major risk factor for crohn's disease, does exist.

But it is not diet, but acute gastroenteritis and the subsequent development of crohn's disease.

Increased Short- and Long-Term Risk of Inflammatory Bowel Disease After Salmonella or Campylobacter Gastroenteritis.

https://www.sciencedirect.com/science/article/abs/pii/S0016508509005241?via=ihub

Infectious Gastroenteritis and Risk of Developing Inflammatory Bowel Disease

https://www.sciencedirect.com/science/article/abs/pii/S0016508508009578?via=ihub

Acute Gastroenteritis Is Followed by an Increased Risk of Inflammatory Bowel Disease

https://www.sciencedirect.com/science/article/abs/pii/S0016508506002629?via=ihub

 

[asadmom]

Do you see possible parasite involvement in CD at all?

 

[kiny]

Parasites infections are common in the developing world. Crohn's disease is primarily a Western disease, slightly more prevalent in urban environments and among the "upper class". So I don't really, there's no reason to suspect parasites.

The opposite has been suggested a few years ago. A lack of helminth and hookworm exposure in the Western world resulting in an underdevelopment of the immune system, the so called "hygiene theory". But it's hard to know if these theories have merit, parasite infections did go down drastically in the Western world, and it matches the increase in certain intestinal disease. But so does refridgeration, the so-called "cold chain hypothesis". Both the "hygiene theory" and the "cold-chain hypothesis" are interesting theories though.

The "hygiene theory" is the idea that lack of early exposure to pathogens in early childhood results in an underdeveloped immune system. I think a bit of a flaw in this theory for crohn's disease, is that migrants from underdeveloped regions who migrate to the Western world, develop crohn's disease at rates similar, or even higher, as the local population. The lack of hygiene and exposure to pathogens in their early childhood does not seem to confer them protection.

The "cold chain hypothesis" has more merit I think, because we see salmonella and campylobacter infections are a major risk factor for developing crohn's disease. This has been confirmed in very large studies in both the US and Europe. Foodborne infections are surprisingly common in the Western world.

Anthony Segal suspected foodborne infections were involved. So did Van Kruiningen to explain the clustering of crohn's disease he noticed in France and Belgium. These large studies confirm their beliefs.

There used to be many more people on the forum. I once made a thread asking if onset of disease in people was accompanied with fevers, night sweats, throwing up, etc. I wanted to know how acute onset of crohn's disease was. Many people answered positive to the question. Because crohn's disease is an acute event, diet is likely not the trigger, but it is far more likely to be an acute infection.

 

[kiny]

The best epidemiology clues are found in studies from the 80s, and the recent large studies that associated acute gastroenteritis infections with crohn's disease.


Anthony Segal showed the innate immune response in crohn's disease is delayed compared to controls.

Anthony Segal showed elemental nutrition causes remission.

Van Kruiningen showed crohn's disease happens in clusters and there is an environmental factor.

Van Kruiningen and others showed migrants from developing countries with low rates of Crohn's disease develop crohn's disease at rates similar or higher than the local population after migration.

Rutgeerts and Harper showed fecal matters that comes into contant with previously unaffected intestinal tissue results in inflammation in crohn's disease patients. When this fecal matters is filtered by an ultrafiltrate, the challenge with intestinal tissue shows no inflammition at all, which shows a large dietary particle or bacteria/fungi is involved.

Large studies in both the US and Europe show crohn's disease is much more common after an acute gastroenteritis infection.

Studies show invasive E Coli thrive in the inflammatory conditions of crohn's disease and exacerbate inflammation.

Klebsiella and other pathogens are found to be more common in crohn's disease patients.

 

[kiny]

Rutgeerts is where the "Rutgeerts score" comes from.

He also made a study called "To cut is not to cure".

Meaning...surgery does not cure the disease. Arguing against surgery where possible, because the disease will simply reappear in previously unaffected tissue.

There was still some belief among some GI that surgery would simply result in a cure. This was not the case and Rutgeerts made sure to tell everyone.

This is when many GI realized that they should contain the disease, and we should avoid surgery at all cost.

Control inflammation, avoid surgery, do not harm the patient ... this is the main goal .. the cure will come one day.

 

[asadmom]

Kiny, who or which lab in the field right now is just like these researchers from the past that are bright, have the right aim, conduct proper research, not in the big pharma's back pocket and align themselves only with capable collaborators to always speak the truth? I want to know who really acknowledges the urgency and is capable to move the needle for the patients? Are they on twitter? How can we support?

 

[kiny]

Coombes lab, lab M2iSH and a lab at Nestlé are focused specifically on crohn's disease. All of them are well funded, which is a good thing.

 

[kiny]

If people with crohn's disease limit fiber intake and use EN to manage their disease, the discovery of a dysbiotic microbiome where fiber-fermenting bacteria were reduced in patients, is not at all abnormal. But a result of dietary changes.

If inflammation subsides with EN, SCD, low residue or low-FODMAP diets due to the lack or complete absence of fiber in all of these, these patients should not be told by dieticians to increase fiber content, especially prebiotics which rely on inulin should be avoided.

The theoretical benefit of fiber fermenting bacteria to produce SCFA / butyrate is completely meaningless in respect to the ability to mediate inflammation by limiting fiber. Even in IBS this would not be a reasonable trade-off.

 

[Andersen007]

Intriguing theory Kiny, but if bacterial fermentation is to blame how come most studies done on low fodmap diet and IBD show that it has no significant effect on inflammation, and in clinical practice only really used to help overlapping IBS symptoms?

 

[Andersen007]

And perhaps I should add, I am asking this after farting my way through a day after consuming a single banana yesterday. So it's not unreasonable, but because I am already on SCD, I would need a lot of mental fortitude to go for low fodmap too to see if it helps my ongoing flare. And so far I didn't find that many promising things that would prompt me to go all-in for low fodmap too.

 

[Andersen007]

Also one more thought.. this study you linked yesterday here: https://crohnsforum.com/threads/pre...fibre-do-not-impact-effectivness-of-en.87321/
also seems to suggest that actually the EEN may or may not have fiber and / or starch, it will still be effective. So how do you piece this all together?

 

[kiny]

EN contain no, or little to no, fiber.

-82% Of the 61 formulas had 0 fibre.
-18% had little to no fiber, far less than a normal diet would contain.

There's no suggestion being made in that study that these EN would stil remain effective after adding fiber to them.

 

[Andersen007]

And what about those studies around vegetarian / vegan / semivegetarian diets, even though on relatively small samples, that seem to strongly indicate the efficacy of these diets full of fibre? There seems to be quite a few out there:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2877178/https://tp.amegroups.org/article/view/23036/22512

 

[kiny]

The most abundant amino acid in the body is glutamine, the biggest users of glutamine are intestinal tissue and immune cells. Those epithelial cells in the intestine, and the tight junctions protein keeping everything from falling apart, are renewed every couple of days. This whole process depends on ample access to protein and growth factors.

A vegetarian or vegan lifestyle is great if you don't have a disease, get B12 shots to make up for the inevitable defficiency you will develop, but it's not recommended at all for crohn's disease due to the danger of protein defficiency.

 

[kiny]

Rutgeerts has laid much of the groundwork regarding research in Crohn's disease. One of the earliest studies he did was trying to give his crohn's disease patients extra glutamine. Most people with crohn's disease are actually not protein defficient, and have ample access to free glutamine in the body. But in patients where access to glutamine is restricted through certain diets or lifestyles, atrophy of the intestine occurs, common in malnourished populations in 3rd world countries due to a lack of access to protein.

 

[kiny]

seem to strongly indicate the efficacy of these diets full of fibre? There seems to be quite a few out there:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2877178/

The patients received infliximab.

Mitsuro Chiba has been advocating for these plant based diets in his studies which usually have a sample size of ≤5, no control group and the patients are either on anti-TNF or other medication. It's not the first time he is discussed on the forum.

He can't induce remission in patients with this diet, but claims after induction of remission with biologics, his diet maintains remissions.

He makes podcasts, is active on forums, he has more pictures of his meals than most restaurants have dishes. His whole argument revolves around the idea that a Westernized diet is to blame for the cases of crohn's disease in Japan.

And that doesn't mean he can't be right, maybe he is. But these studies aren't very reliable, the person behind them has a preconceived notion which taints the studies.

 

[kiny]

For what it's worth, inducing remission with anti-TNF and then relying on diet or lesser medication, which is what he does, is not at all a strange concept. His studies are simply not reliable because of the small sample size, lack of controls, and all his preconceived notions that taint his group's studies.

Infliximab was the first biologic and it was initially never given every 8 weeks. TNF stands for tumor necrosis factor and fulfills important immune functions, there was no confidence at all that you could give this multiple times.

Infliximab was administered once to induce remission and immediately discontinued.

 

[Andersen007]

Another pretty big doubt I have on your fiber theory is, SCD itself excludes starches - that EEN-s do tend to have - and includes plenty of fiber - that EEN does not typically have. And it's not as successful, but still quite a decent diet that's well proven for Crohn's.

 

[kiny]

SCD itself excludes starches - that EEN-s do tend to have

EN don't have natural starches. Maltodextrin or equivalent glucose syrups are starch hydrolysates, they're glucose that get readily taken up. They have nothing to do with starches anymore after the long hydrolysis processing.

If these EN used for crohn's disease actually had natural starches, you'd have a real problem on your hands, because it would no longer be water soluble, and using it intravenous would get you fired.

 

[kiny]

Btw, regarding the study and our friend Mitsuro Chiba.

A small non-exhaustive list of his studies released in the last few years.

That's just those regarding crohn's and UC, he claims to have solved several disease wtih plant-based interventions and diets.

You think maybe he has some preconceived notion about plants. I think he is up to 40+ studies regarding plant and vegetarian solution to diseases.

Checking the authors behind studies and their previous work is just as important as the study itself.

"Incorporation of Plant-Based Diet Surpasses Current Standards in Therapeutic Outcomes in Inflammatory Bowel Disease
Feb 2023
Mitsuro Chiba

Plant-Based Diet Recommended for Inflammatory Bowel Disease
Mar 2023
Mitsuro Chiba

Infliximab and Plant-Based Diet as First-Line Therapy Followed by Corticosteroid Therapy for Severe Ulcerative Colitis: A Case Report
Sep 2022
Mitsuro Chiba

Onset of Ulcerative Colitis in a Patient with Type 2 Diabetes: Efficacy of a Plant-Based Diet for Both Diseases
Sep 2022
Mitsuro Chiba

Relapse-Free Course in Nearly Half of Crohn’s Disease Patients With Infliximab and Plant-Based Diet as First-Line Therapy: A Single-Group Trial
Jun 2022
Mitsuro Chiba

Efficacy of a Plant-based Diet (Semi-lacto-ovo-vegetarian Diet) for Treating Constipation
Dec 2021
Mitsuro Chiba

Stepwise Treatment With Plant-Based Diet and Medication for Patient With Mild Ulcerative Colitis
Dec 2021
Mitsuro Chiba

Increased Incidence of Inflammatory Bowel Disease in Association with Dietary Transition (Westernization) in Japan
Oct 2021
Mitsuro Chiba

Appendiceal Orifice Inflammation in Severe Ulcerative Colitis and Its Resolution With Infliximab and Plant-based Diet as First-line Therapy
Jul 2021
Mitsuro Chiba

High Remission Rate with Infliximab and Plant-Based Diet as First-Line (IPF) Therapy for Severe Ulcerative Colitis
Nov 2020
Mitsuro Chiba

How to Optimize Effects of Infliximab in Inflammatory Bowel Disease: Incorporation of a Plant-Based Diet
Apr 2020
Mitsuro Chiba

Recommendation of plant-based diets for inflammatory bowel disease
Jan 2019
Mitsuro Chiba

Onset of Ulcerative Colitis in the Second Trimester after Emesis Gravidarum: Treatment with Plant-based Diet
Apr 2018
Mitsuro Chiba

Induction with Infliximab and a Plant-Based Diet as First-Line (IPF) Therapy for Crohn Disease: A Single-Group Trial
Dec 2017
Mitsuro Chiba

Development and Application of a Plant-Based Diet Scoring System for Japanese Patients with Inflammatory Bowel Disease
Oct 2016
Mitsuro Chiba

Onset of Ulcerative Colitis during a Low-Carbohydrate Weight-Loss Diet and Treatment with a Plant-Based Diet: A Case Report
Jan 2016
Mitsuro Chiba

High Amount of Dietary Fiber Not Harmful But Favorable for Crohn Disease
Feb 2015
Mitsuro Chiba

From Low-Residue Diets to Plant-Based Diets in Inflammatory Bowel Disease
Oct 2014
Mitsuro Chiba

Lifestyle-related disease in Crohn’s disease: Relapse prevention by a semi-vegetarian diet
May 2010
Mitsuro Chiba "