Thinking about Crohn's wrong has set patients back decades

[Pangolin]

The near-exclusive focus on Crohn's as an immune disorder has clouded the judgment of doctors and has set back the research on Crohn's by at least a decade. Even today, many if not most doctors consider Crohn's to be an autoimmune disorder, although little evidence in favor of that theory has ever been produced.

Yes, Crohn's is characterized by an immune response (inflammation), but that doesn't mean that the immune system is the root of the problem. Yes, patients can be helped by various kinds of immune-suppressing and immune pathway-blocking drugs, but none of this means that causation starts with the immune system going wrong. The entire industry has been based on this assumption that Crohn's is caused by some kind of immune system problem, even though there's no actual proof.

I believe if doctors had a more appropriate mindset about Crohn's and humility about what we know and don't know about it, patients would receive better treatment. If the pharmaceutical companies hadn't been so laser-focused on blocking the next immune pathway for the last 30 years, maybe we would be seeing more progress toward real solutions.

I don't know exactly what causes Crohn's. I have my favored perspective (damage-oriented), but there are other possibilities. The bacteria-focused theories like MAP and AIEC deserve much more investigation than they've gotten so far. It's just sad that nearly all the focus has been on blocking the immune system for the last 30+ years.

 

[Carabop]

I agree with you Pangolin. I try to tell my doctor this and they get upset with me. The money is in the medicine not a cure.

 

[James02]

Do people suspect Crohn's could be driven by a food sensitivity or allergy causing the immune response? Just curious as I'm newer to the forums and Crohn's.

 

[Bufford]

Its hard dealing with a GI who has tunnel vision due to the theory of biologics being the only answer. My experience of biologics has left my body in a miriad of horrible side effects. I will have nothing to do with these treatments, and it does not help any when the GI will not look beyond biologics. It leaves the patient helpless. Given the huge costs of administering biologics I feel that it is being driven by big pharma and profits.

 

[Pangolin]

Do people suspect Crohn's could be driven by a food sensitivity or allergy causing the immune response? Just curious as I'm newer to the forums and Crohn's.

There is no consensus. However, there is a lot of evidence that food has something to do with the causation. Food allergies could be part of the causation in some cases, but my guess is that it's more often related to chemical damage caused by certain food components eg frying oils.

Nothing has really been proven, though.

 

[James02]

@Pangolin Thanks - I've done some elimination diets but nothing really stood out. For me, finding key foods that trouble me are tough. Ugh.

 

[my little penguin]

@James02
True food allergies IgE mediated -occur within two hours of consuming the food
These can cause anaphylaxis or anaphylactic shock and lead to death
These do not cause crohns

food sensitivities are a different ball of wax
They can cause Gi upset among other things and the jury is out on them

cded ,scd ,and een are all peer reviewed accepted “diets “ with intent to treat in crohns
Success varies among folks
Een (exclusive enteral nutrition-formula only no solid foods ) is used a lot in kids to calm inflammation while waiting for meds

cded has been used in kids and adults who were refractory to other meds
Sometimes it works
https://www.ntforibd.org/what-is-nu...rapeutic-diets/crohns-disease-exclusion-diet/
What is a trigger food can and does change depending on whether your flaring or not
And sometimes just changes for no reason
After 11 years of dealing with my child having this nothing surprises me anymore


good luck

 

[Carabop]

Its hard dealing with a GI who has tunnel vision due to the theory of biologics being the only answer. My experience of biologics has left my body in a miriad of horrible side effects. I will have nothing to do with these treatments, and it does not help any when the GI will not look beyond biologics. It leaves the patient helpless. Given the huge costs of administering biologics I feel that it is being driven by big pharma and profits.

All GI’s I have seen have had this tunnel vision. These are the only drugs they ever offer me even when I ask if there is anything else.

 

[James02]

@James02

cded ,scd ,and een are all peer reviewed accepted “diets “ with intent to treat in crohns
Success varies among folks
Een (exclusive enteral nutrition-formula only no solid foods ) is used a lot in kids to calm inflammation while waiting for meds

Wow - I am reading up on these. That link looks very interesting. I was aware that Paleo's diet was helpful (due to reading on this forum), but I'm not familiar with the CDED, EED. I'll take a peek.

Thank you!

 

[westernbuddy]

Gi or doctor will tend to offer the patient the best medicine they have at the time.

98% of Gi's are not scientists or pharma companies.

20 years ago medicine was very limited, biologics have given them more options.

They are perfectly aware of the disease and all its unknowns. But when a sick patient turns up they do what they can.

So I don't think it can be taken out on the patient facing Gi.

Outside of the gi world science and medicine/pharma is very complex.

Subjects like this raise awareness power of the people.

I know lots of scientists and Gi's are hopeful newer and safer medicine will come for our disease.

There is a really huge amount of work being done in the IBD area now. We may have hope, but not for another decade I don't think at least.

 

[kiny]

Do people suspect Crohn's could be driven by a food sensitivity or allergy causing the immune response?

A food allergy or sensitivity would evoke an immune response everywhere where the allergen comes into contact with the epithelial cell wall.

That is not the case in crohn's disease, crohn's disease occurs exclusively in areas with high bacterial load like the ileum and colon. The oral cavity is the only other area with high bacterial load, and not surprisingly people with crohn's disease frequently develop aphthous ulcers in their mouth.

In places where bacteria live and are able to penetrate into deeper lamina propria tissue, crohn's disease manifests itself. In places with low bacterial load, like the upper GI tract, crohn's disease is completely absent.

Early symptoms of crohn's disease features patchy skip lesions in ileal tissue surrounding points of entry for bacterial antigen, like the peyer's patches.

Crohn's is bacterial.

Immunosupressants control the cascading inflammation due to bacterial entry into tissue and the proliferation of bacteria like AIEC that replicate inside macrophages, but it does not address the cause. The cause being pathogenic bacteria that are able to enter tissue, evoking a chronic immune response due to the inability of the immune system to clear these bacteria.

 

[kiny]

What you can argue of course is that Western diets promote an environment whereby pathogenic bacterial populations in the intestine gain the upper hand.

But this is something very different from a food allergy, an allergen creates inflammation everywhere it comes into contact with tissue immune cells. If you skin is allergic to nickel your nickel watch will cause an immune response regardless if you put the watch on your wrist or around your ankels. A nut allergy will cause an immune response everywhere the allergen comes into contact with epithelial cells, from the epidermis of your skin to the epithelial cells in your throat.

This is of course not what is going on in crohn's disease.

Crohn's disease features very specific skip lesions in areas with high bacterial load, it's not caused due to an allergy against some foods. If it was an allergy, you would have inflammation everywhere, you don't.

 

[kiny]

If you ask yourself what crohn's disease looks like, it doesn't look like an allergic reaction, it certainly doesn't look like UC.

What it does look like is intestinal TB, it looks like chronic granulomatous disease, it looks like a chronic foodborne infection. You can see inflamed peyer's patches, you can see granuloma featuring macrophages trying to shield off bacterial entry. You can see the innate immune system with activated macrophages release cytokine like TNF-alpha, you can see a very active and chronic adaptive response.

What I see, is an unresolved bacterial infection that became chronic.

 

[kiny]

What crohn's disease also is not, is an immune response against the microbiome. For one, you would have inflammation everywhere where the microbiome touches the epithelial wall, that is not the case. And secondly, the microbiome surrounding early ulcers in crohn's disease, is not dysbiotic, dysbiosis developes later (likely due to the inflammatory conditions). This dysbiosis largely dissapears in people in remission, but it does not cure the disease. Nor do fecal transplants or microbiome interventions cure the disease (they tend to make the inflammation worse). Dysbiosis is a feature of crohn's disease, likely due to the inflammatory condition, but it is clearly not the cause and the inflammatory response is clearly not targeting the microbiome.

What is the most likely explanation, is that a pathogenic bacteria gained entry into tissue (either through tight junction failure or M cells), and set off a tissue immune reponse in the lamina propria.

As long as these bacteria manage to evade the immune system and are not cleared, inflammation will persist. Not very different from how some people in remote areas of the world with intestinal TB would suffer for years before treatment cleared the bacterial infection.

 

[kiny]

As far as possible candidates for those pathogenic bacteria, there aren't that many bacteria that can enter through peyer's patches and evade the immune system.
-pathogenic E Coli (AIEC)
-klebsiella
-foodborne infection like salmonella, campylobacter
-mycobacteria
-fungi

A viral infection is very unlikely simply because there is no precedent for this. Bacteriophages have evolved in harmony with humans, I have never heard of them actively causing disease, they don't infect cells. Viral gastroenteritis doesn't look like crohn's disease at all.

 

[westernbuddy]

And then when you have chronic inflmation and ulcers, you start eating foods that annoy the tissue even further, pouring alcohol onto cut swollen inflamed tissue, then feeds the fire and leads to further damage.

I feel my dudoneum and ileum talking to each other, as I have a stricture in both, bacteria feels right, if feels often like they are trying to pass the buck to each other.

The lilium will say we are tired, dudboeum please hold the food some longer don't let bacteria down yet, then the duconeum has overload. Then the fight begins with the dudoneum and ilium, that's how I feel it.

 

[Pangolin]

Kiny, I agree with you that the inflammation in Crohn's is primarily an immune response to bacteria. However, there are many unanswered questions about exactly which bacteria (my guess is it's not just AIEC), why some patients get sick and others don't when most people are probably commonly exposed to these bacteria, how the bacteria are getting exposed to the immune system in certain places, why the problem becomes chronic in Crohn's patients, whether we can eliminate these bacteria, and whether patients have long-term improvement after the bacteria is eliminated.

What is it about Crohn's patients that results in these problems, while other people similarly exposed to bacteria have no problems? I presume that we would notice that Crohn's is infectious if the answer were simply that Crohn's patients get exposed to a specific bacteria and others don't.

I also suspect that the answer to this question is not "Most Crohn's patients have defects of the immune system", because I think that also would have been figured out by now. This is why physical or chemical damage or structural issues in the intestine or wound healing problems come up in my thinking, to explain what it is that makes certain people vulnerable.

On the other hand, maybe it's more like stomach ulcers and H.Pylori, and maybe just getting rid of the bacteria is the key.

 

[kiny]

However, there are many unanswered questions about exactly which bacteria (my guess is it's not just AIEC), why some patients get sick and others don't

We can now accurately predict who has a high chance of developing crohn's disease by using anti-OmpC and anti-flagellin serum tests, that indicate these people carry pathogenic E coli. Note that this only works for crohn's disease, not UC.

https://pubmed.ncbi.nlm.nih.gov/32165208/

What is it about Crohn's patients that results in these problems, while other people similarly exposed to bacteria have no problems?

It's just a roll of the dice.

A lot of infections happen as co-infections, where a primary infection serves as a precursor for the secondary infection.

A bacteria just needs the right conditions to thrive.

We see people often develop crohn's disease after a foodborne infection like campylobacter or salmonella. It leaves the intestine permeable, allowing a pathogenic bacteria to enter tissue.

We see people often develop crohn's disease after a course of antibiotics. Antibiotics gives a fitness advantage to pathogic species. After a course of antibiotics, they are no longer in competition with other bacteria, and can now attach themselves to an epithelial wall and invade tissue.

A number of people with crohn's disease have genetic anomalies that diminish phagocytosis competence of macrophages, which intracellular bacteria exploit.

 

[kiny]

On the other hand, maybe it's more like stomach ulcers and H.Pylori, and maybe just getting rid of the bacteria is the key.

In 1998 a researcher in Clermont-Ferrand in France discovered AIEC. Darfeuille-Michaud.

The reason it took such a long time before this bacteria got the spotlight it deserves, with large studies now found in journals like Nature, is because these bacteria are new, and need to be classified through virulence and adhesion properties because they have no easily identifable genetic marker.

If we can identify the troublemakers in crohn's, remove them with phages or disarm them with fimH blockers or anti-adhesion molecules, we are well on our way to new treatments that will be much more effective.

 

[Pangolin]

We can now accurately predict who has a high chance of developing crohn's disease by using anti-OmpC and anti-flagellin serum tests, that indicate these people carry pathogenic E coli. Note that this only works for crohn's disease, not UC.

This proves that the immune system is reacting to certain bacteria, but what we don't know is whether this is a cause or an effect of the inflammation. Perhaps the inflammation (or, say, a defect in the intestinal lining caused by a prior infection) causes changes in the gut that allow bacteria to get exposed to the immune system, which results in the immune reaction. Perhaps a normal intestine doesn't allow the bacteria to become exposed to the immune system in the first place. My guess is you need the bacteria *and* an abnormality that exposes the immune system to the bacteria, and then the process can begin.

The usual problem with these theories, eg MAP, is that we can notice that we find MAP much more commonly in people with Crohn's, but we just don't know if that's merely because MAP thrives in the intestinal conditions of a Crohn's patient, because MAP is causing the inflammation, or because any bacteria will cause the inflammation and MAP happens to be there.

We could test this by attempting to induce Crohn's in healthy test subjects by giving them Crohn's associated bacteria, and we could compare them to people who we induce some kind of intestinal lesions in and then expose them to the bacteria, vs healthy controls given placebo. On second thought, maybe we shouldn't do this.

Of course, we do know that reducing bacteria can help some Crohn's patients, and we know that reducing the inflammatory response can also help some Crohn's patients. Maybe any bacterial or inflammation reduction can help the body heal, which reduces future immune system exposure to bacteria, if complete healing does happen. We're not sure yet if we can target and eliminate AIEC or maybe eliminate the specific immune response to AIEC to get rid of Crohn's, and I'm surprised there's no definitive answer to this considering AIEC has been known about for quite a while. Maybe targeting AIEC will really work, though.

A lot of infections happen as co-infections, where a primary infection serves as a precursor for the secondary infection.

A bacteria just needs the right conditions to thrive.

We see people often develop crohn's disease after a foodborne infection like campylobacter or salmonella. It leaves the intestine permeable, allowing a pathogenic bacteria to enter tissue.

We see people often develop crohn's disease after a course of antibiotics. Antibiotics gives a fitness advantage to pathogic species. After a course of antibiotics, they are no longer in competition with other bacteria, and can now attach themselves to an epithelial wall and invade tissue.

A number of people with crohn's disease have genetic anomalies that diminish phagocytosis competence of macrophages, which intracellular bacteria exploit.

Right, I appreciate all of this research. I think this is all on a much better track than the simpler "let's just block the next immune pathway" school of thought.

 

[kiny]

We could test this by attempting to induce Crohn's in healthy test subjects by giving them Crohn's associated bacteria, and we could compare them to people who we induce some kind of intestinal lesions in and then expose them to the bacteria, vs healthy controls given placebo. On second thought, maybe we shouldn't do this.

In the 90s Rutgeerts and Harper did such experiments. Rutgeerts showed that crohn's disease develops when healthy intestinal tissue from crohn's disease patients comes into contact with intestinal fluids. Harper redid this experiment and came to the same conclusion, but when Harper filtered out all the bacteria from the intestial fluids, no inflammation was observed.

Early lesions of recurrent Crohn's disease caused by infusion of intestinal contents in excluded ileum

Background & aims: Postoperative recurrence of Crohn's disease may be triggered by agents in the fecal stream. The aim of this study was to examine intestinal mucosal inflammation induced by contact with intestinal fluids in surgically excluded ileum.

Methods: The effects of infusion of intestinal luminal contents into excluded ileum in 3 patients with Crohn's disease who had undergone a curative ileocolonic resection with ileocolonic anastomosis and temporary protective proximal loop ileostomy were studied by histopathology and electron microscopy.

Results: Contact with intestinal fluids for 8 days induced focal infiltration of mononuclear cells, eosinophils, and polymorphonuclear cells in the lamina propria, small vessels, and epithelium in the excluded neoterminal ileum that was previously normal. Epithelial HLA-DR expression increased, and mononuclear cells expressed the KP-1 antigen associated with activation. Marked up-regulation of RFD-7, RFD-9, intercellular adhesion molecule 1, and lymphocyte function-associated antigen 1 was observed after infusion, reflecting epithelioid transformation and transendothelial lymphocyte recruitment. At the ultrastructural level, dilatation of the endoplasmic reticulum and Golgi apparatus occurred in epithelial cells, where also basally located transport vesicles were identified.

 

[kiny]

Perhaps a normal intestine doesn't allow the bacteria to become exposed to the immune system in the first place.

Bacteria in crohn's disease patients are either entering through M cells or through incompetent tight junctions. In people with ileal disease, they are almost certainly entering through M cells, because that's where all the peyer's patches are. In people with colonic disease they are likely exploiting a general barrier and tight junction failure.

The bacteria causing disease in crohn's disease are highly pathogenic and have clearly invaded tissue, they have been taken up by macrophages, because the inflammation in crohn's disease is deep transmural inflammation. Crohn's disease inflammation is very different from UC inflammation, inflammation in UC is very superficial, in crohn's disease it is deep tissue inflammation that comes from immune cells in the lamina propria, mostly macrophages.

 

[Pangolin]

The fecal stream experiments are great, but they don't tell us why some people are susceptible while others aren't. Would healthy people react the same way to the fecal stream?

Is Crohn's due to ubiquitous bacteria that only affect some people due to particular susceptibilities, or is Crohn's more a result of uncommon exposure to particular bacteria? If the situation is mostly the former, then eliminating the bacteria may not do much because people will just be exposed to it over and over again.

 

[griffis]

Hi,kiny
If AIEC is troublemaker,how to explain pen can Induction of ease?
@kiny

 

[kiny]

Hi, I assume EN works in crohn's disease by limiting bacterial load in the intestine, which would explain why EN is also effective in treating SIBO.

EN is made up of bioavailable glucose syrups, MCTs and broken down proteins that get taken up higher in the intestinal tract than a normal diet would. I believe EN deprives bacteria in the ileum and colon of nutrients.

Some suggest EN works by restoring nutritional deficiencies. I don't think that's the reason, we've tried everything from giving people glutamine, to growth factors, to vitamins, none of them bring down inflation.

 

[kiny]

Another suggestion has been that EN helps restore a healthy microbiome. But that's not what happens, every study points out EN lowers bacterial diversity and worsens dysbiosis.

Yet inflammation rapidly subsides when people with crohn's disease go on EN. The fact EN worsens dysbiosis and lowers bacterial diversity to such an extent, yet inflammation subsides, shows dysbiosis is not behind the inflammation in crohn's disease, and research on the microbiome has too many shortcomings to base any diet on it.

The billions spent on microbiome research has not benefitted a single crohn's disease patient, quite the contrary. Crohn's disease patients are reacting to pathogens, not harmless commensals. That's why fecal transplants and probiotics don't work at all, but macrophage-penetrating antibiotics bring down inflammation.

 

[kiny]

Most researchers and doctors have come around and accepted crohn's disease is a response to bacteria.

Sceptics often ask 2 questions.

"If crohn's disease is related to bacteria, why don't antibiotics cure it?"

Not all diseases caused by bacteria can be cured with antibiotics. More and more bacteria are resistant to antibiotics. Resistant UTI involving E coli can not easily be cured with antibiotics anymore.

"If crohn's disease is related to bacteria, why don't anti-inflammatories make it worse?"

Many bacteria thrive in inflammatory conditions, studies have shown that anti-TNF limit replication of crohn's disease related bacteria in macrophages. Many anti-inflammatories were specifically designed to be used during bacterial infections to limit necrotic tissue and nerve damage.

While anti-inflammatories can be dangerous during acute infections (that's why people get a mantoux test before they are allowed to go on anti-TNF), they are very useful during chronic infections to stop inflammaton from doing long term tissue and nerve damage.

 

[asadmom]

Another suggestion has been that EN helps restore a healthy microbiome. But that's not what happens, every study points out EN lowers bacterial diversity and worsens dysbiosis.

Yet inflammation rapidly subsides when people with crohn's disease go on EN. The fact EN worsens dysbiosis and lowers bacterial diversity to such an extent, yet inflammation subsides, shows dysbiosis is not behind the inflammation in crohn's disease, and research on the microbiome has too many shortcomings to base any diet on it.

The billions spent on microbiome research has not benefitted a single crohn's disease patient, quite the contrary. Crohn's disease patients are reacting to pathogens, not harmless commensals. That's why fecal transplants and probiotics don't work at all, but macrophage-penetrating antibiotics bring down inflammation.

Does that mean that a diet of a very diverse menu (like Mediterranean Diet) is not beneficial to the patients then? Lately there's a lot of push to eat a variety type of food hoping to build a diverse bacteria population and it sounds like that is not what we want. If lowering bacterial diversity is key, then I would assume a simpler diet plan is the way to go for CD patients?

 

[Steiconi]

I'm reading "The Inflammation Spectrum" by Dr. Will Cole. I don't know much about him, just came across the book. Some of what he says makes a lot of sense, like, we each have personalized triggers; something that helps one person may harm another.

His main elimination diet has you cut out grains, dairy, all kinds of sweeteners, and processed oils. A secondary elimination diet includes cutting out legumes, nuts and seeds, eggs, and nightshades. You don't eat them for 4 to 8 weeks, then add one in and see how you do.

I've been doing low carb since January, and mostly cut out grains, sugars, or legumes. I do eat a lot of eggs, cheese, and nuts, so those will be the tough ones for me.

My Crohn's disease has never been debilitating, and I have never taken drugs for it (couldn't see paying $1000 for one month of drugs that had only a 30% chance of working). But it has gotten better since I was diagnosed; some foods are definitely triggers, and I've had good results avoiding them (and bad results when I eat them).

 

[asadmom]

I'm reading "The Inflammation Spectrum" by Dr. Will Cole. I don't know much about him, just came across the book. Some of what he says makes a lot of sense, like, we each have personalized triggers; something that helps one person may harm another.

His main elimination diet has you cut out grains, dairy, all kinds of sweeteners, and processed oils. A secondary elimination diet includes cutting out legumes, nuts and seeds, eggs, and nightshades. You don't eat them for 4 to 8 weeks, then add one in and see how you do.

I've been doing low carb since January, and mostly cut out grains, sugars, or legumes. I do eat a lot of eggs, cheese, and nuts, so those will be the tough ones for me.

My Crohn's disease has never been debilitating, and I have never taken drugs for it (couldn't see paying $1000 for one month of drugs that had only a 30% chance of working). But it has gotten better since I was diagnosed; some foods are definitely triggers, and I've had good results avoiding them (and bad results when I eat them).

So you mainly just manage it by diet only? How do you monitor the disease progression (frequent testing?)

 

[Steiconi]

No labs, I just watch my symptoms--diarrhea, blood, a rash. Blood and rash are gone, diarrhea is sporadic, I think caused by certain foods. Almonds, ice cream, oatmeal all give me problems.

I got the worst gastroenterologist; he didn't tell me much, didn't respond to phone calls or emails. He walked out on me when I came for an appointment because some info was missing from my chart. I gave up waiting after 20 minutes; he'd already been an hour late, and I was raging mad. Pretty much everything I had done with him got screwed up by his office staff. For instance, I was told to show up for a colonoscopy at 6am. I was on time, but they hadn't put me on the schedule, so I had to wait 2 hours until his office opened.

Are you sorry you asked? It's a sore topic with me.

I've looked at online food lists and try eliminating some stuff, adding in supplements. I found https://www.biohmhealth.com by reading "Mycobiome" and used their probiotics for a few months. Maybe those helped, or maybe it was all diet. Currently, I'm taking marshmallow root; it's supposed to soothe the gut. I don't remember where I read that...

 

[kiny]

If lowering bacterial diversity is key, then I would assume a simpler diet plan is the way to go for CD patients?

Less bacterial diversity and increased dysbiosis is a side effect of patients using EN. I don't believe that's how EN brings down inflammation.

What is more likely is that EN brings down inflammation by bringing downs bacterial load. Bacterial load is higher in the ileum and colon, when you switch to EN that is readily absorbed higher up in the intestine, you deprive these bacteria of nutrients.

The fact patients improve on EN, even though their microbiome has become much more dysbiotic, shows dysbiosis is clearly not a factor driving inflammation in crohn's disease patients.

All these interventions trying to manipulate the microbiome like diets, probiotics, fecal transplants, have all been very unsuccessful in treating crohn's disease.

EN and IV feeds, which deprive nutrients to bacteria in the lower intestines, are successful. EN have consistently shown they can drastically bring down inflammation in crohn's disease patients. But it certainly doesn't do this by "restoring a healthy microbiome", the microbiome of patients on EN becomes extremely dysbiotic, yet patients improve.

 

[kiny]

Crohn's disease manifests itself in areas with high bacterial load.

Ileum, Colon. Also in the mouth through aphthous ulcers.

Crohn's disease doesn't manifest itself in the jejunum, duodenum, stomach or esophagus where bacterial load is exponentially lower. The claim that crohn's manifests itself anywhere in the digestive tract is irresponsible and misleading, this is simply not the case. The overwhelming number of patients diagnosed with crohn's disease have inflammation in the ileum or colon, and no inflammation higher up the intestine.

I am highly sceptical of the few patients with local inflammation in the jejunum or duodenum being diagnosed with crohn's disease, the inflammation in those patients doesn't look anything like the deep transmural inflammation involving granuloma found in crohn's disease patients. The inflammation in these patients is minor, often resolves on its own, they are rediagnosed from having crohn's disease to having idiopathic upper intestinal inflammation.

Bacterial load determines where crohn's disease develops, bacterial load is highest in the ileum and colon, and that's where the disease presents itself.

If you filter out the bacteria in the fecal stream like Rutgeerts had done, if you completely deprive these bacteria of any nutrients through IV feeds, or limit nutrients available to bacteria by using EN, inflammation subsides and the intestine heals. Irrespective of any dybiosis or drop in bacterial diversity this might cause as a side effect.

 

[asadmom]

Crohn's disease manifests itself in areas with high bacterial load.

Ileum, Colon. Also in the mouth through aphthous ulcers.

Crohn's disease doesn't manifest itself in the jejunum, duodenum, stomach or esophagus where bacterial load is exponentially lower. The claim that crohn's manifests itself anywhere in the digestive tract is irresponsible and misleading, this is simply not the case. The overwhelming number of patients diagnosed with crohn's disease have inflammation in the ileum or colon, and no inflammation higher up the intestine.

I am highly sceptical of the few patients with local inflammation in the jejunum or duodenum being diagnosed with crohn's disease, the inflammation in those patients doesn't look anything like the deep transmural inflammation involving granuloma found in crohn's disease patients. The inflammation in these patients is minor, often resolves on its own, they are rediagnosed from having crohn's disease to having idiopathic upper intestinal inflammation.

Bacterial load determines where crohn's disease develops, bacterial load is highest in the ileum and colon, and that's where the disease presents itself.

If you filter out the bacteria in the fecal stream like Rutgeerts had done, if you completely deprive these bacteria of any nutrients through IV feeds, or limit nutrients available to bacteria by using EN, inflammation subsides and the intestine heals. Irrespective of any dybiosis or drop in bacterial diversity this might cause as a side effect.

Thank you so much for your thorough explanation @kiny! I feel I haven't learned anything from the doctors for the past year. I merely go to them for drugs.

So you don't believe CDED or SCD has any merit then (so many trials on CDED)? I often wonder why rice is the enemy in SCD but the main staple in CDED. These two diets contradict each other yet all claim to be effective in managing Crohn's.

Another thing that puzzles me is our docs said Crohn's also attacks the eyes and bones so an annual screening is required. Is this risk completely different from the excessive bacteria load in the gut?

 

[kiny]

So you don't believe CDED or SCD has any merit then (so many trials on CDED)? I often wonder why rice is the enemy in SCD but the main staple in CDED. These two diets contradict each other yet all claim to be effective in managing Crohn's.

The idea behind SCD isn't so bad. It suggests several intestinal diseases are caused by undigested carbohydrates in the intestine that serve as an energy source for bacteria, if we remove those from the diet, it will lower bacterial load and limit the damage these bacteria can do.

But we're in the 21st century, and EN is much more effective at accomplishing this. EN is made from glucosy syrup we get with hydrolysis and is taken up before most of it even reaches the ileum, MCT fats that are much more bioavailable than those found in an SCD diet, and broken down proteins so you don't need to break them down yourself.

The idea behind SCD isn't bad, it's just that we have much more effective ways to increase bioavailability of our diet like EN, or IV feeds.

If we are going to treat Crohn's disease by limiting the availability of nutrients to bacteria, you might as well do it with all the tools we have at our disposal in the 21st century.

 

[kiny]

Another thing that puzzles me is our docs said Crohn's also attacks the eyes and bones so an annual screening is required. Is this risk completely different from the excessive bacteria load in the gut?

I don't think Crohn's disease is like Behcet's disease, where inflammation manifests itself in very different parts of the body.

The aphthous ulcers we see in the mouth of patients with crohn's disease are directly related to the disease itself. But other than that I would be hesitant to attribute anything else to crohn's disease.

Crohn's disease manifests itself in the ileum, colon and mouth. It is pure guesswork if it manifests itself in other areas of the body, I don't think it does.

 

[Ignotius]

i have a few thoughts on this...

regarding EN.....im amazed some that nobody mentioned about low residue perhaps having anything to do with it....

all these diets tho, i feel will focus on some important things and completely ignore others....

for example, rice....and bacterias....and fiber etc...
there are very many types of rice, as well as ways to prepare them....i have landed on sela basmati as the parboiling converts some of the starches to r3, and i still do soaking things as well for minimizing any impurity/antinutrient lvls as much as possible........converting that starch means it isnt absorbed as glucose in small intestine, which surely will effect bacterias........the less inflammation, it seems to me the more fiber can help....by pure regularity even........but anyway yeah, i blend some forbidden rice in for insoluable fiber sort of "as needed" and as well as i have been able to figure out what optimum even is........the more inflamed i tend to go lower residue, less insoluable fiber...

as far as bacterias themselves......my guess on it is, diversity is good, but overpopulation is bad.....diversity helps prevent any certain cultures becoming too dominant.....as well as other assumed benefits........right after my surgery i dosed a few probiotics, but now i cut those out and trying to dare working in some more fruit and veggies...fibers/starches.......then toward preventing over population, idk, but we know there are several things which are at least said to "only kill bad stuff"....aka, monolaurin, quercetin, aged garlic and such...

its worth coming at this from several angles imho.....if the chicken or the egg was first.....i think we have to say leaky gut is a part of this right? there are both chicken and eggs all over the place by now so it doesnt really matter to me the relationship just that there obviously is one....i also take marshmallow root extract for this, and slippery elm as well.....some other things, but it all has to be well understood to get the most from......like how taking these things within 2 hours of nutrition will inhibit uptake etc......i see these all in one supplements and such, because it is easier to market sure but um....are we considering how things actually work and maximizing effects? ....before we say they failed...

so.....modifying these diets, and including amazing things they fail to even mention.....like......millets? hello?

 

[Ignotius]

in regards to eyes and bones tho......i think that comes back to nutrition.....i am sort of at that age anyway mid 40s, but my chrons really killed my lifetime of spectacular vision and my bones and joints certainly became more achey.....joints feel better since i been hardcore about the nutrition but in some parts damage is already done.....like dental issues even that got accelerated....

 

[kiny]

It's certainly possible that nutritional deficiencies related to crohn's disease affect other parts of the body.

But this is different from something like Behcet's disease where you see the inflammation itself affect different parts of the body.

 

[Ignotius]

iv feeds seem bad too......i was 100lbs of my 160lb normal.....pre surgery....could hardly eat anything, not that they were giving me much chance to.....
i thought the obvious idea would be iv nutrition.....if not then, i mean, when?
but i was told it dangerously increases chances of things like fungal infections or such like i guess i wasnt quite life or death enough somehow....even tho i couldnt walk.

it seems like EN and this is a short term benefit to reduce inflammation, but it only makes sense to me as a low residue interaction....and of course balancing/depriving bacterias some but all that starts working against us in the delicate balance of things...long term....

 

[kiny]

The major risk of IV feeding patients is a bloodstream infection. It can only serve as a temporary intervention to get a patient in remission.

 

[patulsius]

@kiny what do you think about the fodmap diet? Do you think it could be useful as a sibo diet to help to reduce the bacterial load?

 

[kiny]

Bacteria have developed lots of strategies to cope with nutritional deprivation, they can remain in a dorment state for a while.

Diets are just not that effective. For all the claims that diets influence bacterial populations in the intestine, these effects seem to be temporary, and populations quickly recover after the dietary intervention is stopped.

Even for SIBO, an overgrowth of bacteria in the small intestine, EN have shown to be much more effective than any diet or even antibiotics in lowering bacterial load and treating SIBO.

 

[Ignotius]

fwiw, ive not been doing fodmaps for....9 months or something?
seriously planning to work some fruit and veggie in more tho...for diversity sake...idk...

i just know before i knew i had chrons, i was looking at things like fodmaps alot more....because i was sensitive to EVERYTHING.

so it does make some sense to me about focusing balance, and adjusting things time to time....im also using things like sac B. or epicor, in addition to the anti viral/bacterials etc. to try and help keep pushing out/balancing "bad cultures"...

interesting conversation anyway.....i only wish it wasnt so hard to apply well thought out plans to research better...

 

[asadmom]

The idea behind SCD isn't so bad. It suggests several intestinal diseases are caused by undigested carbohydrates in the intestine that serve as an energy source for bacteria, if we remove those from the diet, it will lower bacterial load and limit the damage these bacteria can do.

But we're in the 21st century, and EN is much more effective at accomplishing this. EN is made from glucosy syrup we get with hydrolysis and is taken up before most of it even reaches the ileum, MCT fats that are much more bioavailable than those found in an SCD diet, and broken down proteins so you don't need to break them down yourself.

The idea behind SCD isn't bad, it's just that we have much more effective ways to increase bioavailability of our diet like EN, or IV feeds.

If we are going to treat Crohn's disease by limiting the availability of nutrients to bacteria, you might as well do it with all the tools we have at our disposal in the 21st century.

Understood. Are you suggesting EN for maintenance or EN for induction then transition to PEN?

 

[Ignotius]

or about dairy even you know......all this talk......nobody mentions A2.....nobody considers grain/lectin free......but we are just diving right in to how good or not it is???

 

[Scipio]

Crohn's disease manifests itself in the ileum, colon and mouth. It is pure guesswork if it manifests itself in other areas of the body, I don't think it does.

A quick glance at the Extra-Intestinal Manifestations board on this forum will show you that Crohn's affecting parts of the body other than ilieum, colon, and mouth is quite common. In my case the disease first presented in the ileum and stayed there for the first five years after diagnosis, but it then attacked my pericardium inducing restrictive heart failure. The problem was fixed by a combination of surgery to remove the inflamed pericardium and addition of Stelara to better battle the Crohns.

I agree that a bacterial trigger plays a major role in the etiology of most cases of Crohn's, but it's also a very complex disease that can quite commonly throw curve balls. Like lupus, once it gets going Crohn's can manifest itself in highly variable sites and ways.

 

[kiny]

Understood. Are you suggesting EN for maintenance or EN for induction then transition to PEN?

The idea that one doesn't have to adhere to EN, can do partial EN or can mimmick EN with a diet, is a very attractive suggestion.

Any PEN study, or any diets mimicking EN like "CD-Treat", are very popular and regularly shared online.

But when one looks at more rigorous studies, they show PEN and diets mimicking EN are not effective in suppressing inflammation, and are not effective in inducing remission. Unlike exclusive EN.

 

[kiny]

it seems to me the more fiber can help....by pure regularity even

Yeah, there's very little fiber in EN. But this has more to do with the production process of EN than purely trying to avoid fiber.

Some people on the forum have said they get constipation when using EN, that's due to the lack of fiber of course. The few undigested nutrients in EN are likely little amounts of LCT that can be found in EN, undigested fats. Without any fiber this doesn't weigh anything.

There's no reason why one can't eat a little something with fiber in conjunction with EN. EN with 1g of fiber per 100g of EN are just as effective as those with 0g of fiber.

EN have been used to treat crohn's disease since at least as far back as the 1980s (many old studies can be found in journals like the BMJ). What they have always shared is their reliance on glucose, glucose syrups, MCTs and broken down protein. Fiber content, emulsifiers, minerals, and growth factors can differ per EN, but they don't affect their efficacy, they can all induce remission.

 

[asadmom]

The idea that one doesn't have to adhere to EN, can do partial EN or can mimmick EN with a diet, is a very attractive suggestion.

Any PEN study, or any diets mimicking EN like "CD-Treat", are very popular and regularly shared online.

But when one looks at more rigorous studies, they show PEN and diets mimicking EN are not effective in suppressing inflammation, and are not effective in inducing remission. Unlike exclusive EN.

View attachment 4318

But EEN as a maintenance is so tough (is it still doable?). That is basically saying goodbye to chewing food and social events. Can there be a more realistic maintenance diet?

 

[kiny]

Right, the limiting factor for EN is compliance. Studies have tried to add some aromas / tastes to EN to spice them up, which might be an option.

It also depends a bit on the EN, 028 from Nutria is very bitter tasting, Modulen is very sweet tasting.

It's easy to stay on the rails if you don't cheat, the desire to eat solid foods disappears. Once one cheats it is much harder to get that person back on the rails. No different from any other addiction I guess, the first days without solid foods are the most difficult, after a few days the desire to consume solid foods disappears.

 

[asadmom]

Right, the limiting factor for EN is compliance. Studies have tried to add some aromas / tastes to EN to spice them up, which might be an option.

It also depends a bit on the EN, 028 from Nutria is very bitter tasting, Modulen is very sweet tasting.

It's easy to stay on the rails if you don't cheat, the desire to eat solid foods disappears. Once one cheats it is much harder to get that person back on the rails. No different from any other addiction I guess, the first days without solid foods are the most difficult, after a few days the desire to consume solid foods disappears.

It's a daunting task... both physically and mentally that's for sure.

Do we have any long term data on using EEN as maintenance without med? It is a very attractive option for the tough people if it means no biologics.

 

[kiny]

Yes, there's 6 month - 1 year studies on EN, mostly from Japan where EN is much more widely used to treat crohn's disease in adults.

Keep in mind that EN can be used together with medication too. It can avoid a patient having to take an increased dosis for example.

 

[kiny]

Lots of very old studies too, from the 60s and 70s, where EN was used to treat people with former Intestinal TB, these people were often underweight, unable to take up enough nutrients. You can find them in the Lancet and the BMJ. Intestinal TB is rare in the Western world today, we can easily identify and treat this disease today too.

This didn't used to be the case, there were a lot of people with severe damage to their intestine who could no longer properly digest food due to the damage intestinal TB did to their intestine. EN was a solution, not only did it improve the nutritional status of these patients, a lot of affected intestinal tissue was restored, likely a lack of glutamine and other nutrients was reverted when they were given EN.

This is also how the first trial with EN for crohn's disease patients happened, not to treat the disease, but to simply get these underweight patients back on their feet. Of course not much later studies appeared that showed that EN didn't just get underweight patients on their feet, EN actually brought down inflammation and treated the disease.

 

[asadmom]

Kiny, I hope you are practicing medicine somewhere or at least participating in Crohn's research because your knowledge on this subject has and will continue to help others (that come after us, sadly) make informed decisions. Thank you.

 

[westernbuddy]

You should ask your nhs hospital how many patients they have with crohns, and how many they have with it in the dudoneum.

You would be surprised, its far more common than Google portrays, and it leads to lots of strictures, surgery and a bypass,

I have crohns in my dudoneum and ileum and it can get quite bad in both places.

The consultants on the ground will tell you the uk facts on what there dealing with each day

 

[asadmom]

As far as possible candidates for those pathogenic bacteria, there aren't that many bacteria that can enter through peyer's patches and evade the immune system.
-pathogenic E Coli (AIEC)
-klebsiella
-foodborne infection like salmonella, campylobacter
-mycobacteria
-fungi

A viral infection is very unlikely simply because there is no precedent for this. Bacteriophages have evolved in harmony with humans, I have never heard of them actively causing disease, they don't infect cells. Viral gastroenteritis doesn't look like crohn's disease at all.

This is a concern of mine. We use the biologics to calm the immune system but leave the underlining culprit in the gut: bacteria/fungi. What is long term harm at masking the problems? Shouldn't we eradicate the problematic bacteria/fungi?

 

[Scipio]

This is a concern of mine. We use the biologics to calm the immune system but leave the underlining culprit in the gut: bacteria/fungi. What is long term harm at masking the problems? Shouldn't we eradicate the problematic bacteria/fungi?

In theory, yes. Unfortunately, the actual results of this approach haven't lived up to the theory. Except for a few magical docs who claim miracle cures that no one else has been able to replicate, the success of the antibiotic approach has been limited and spotty at best and no more long-lasting than the biologics - requiring very long term (perhaps perpetual) medication.

So for now the biologics remain the most effective tool for inducing remission that we currently have.

 

[asadmom]

In theory, yes. Unfortunately, the actual results of this approach haven't lived up to the theory. Except for a few magical docs who claim miracle cures that no one else has been able to replicate, the success of the antibiotic approach has been limited and spotty at best and no more long-lasting than the biologics - requiring very long term (perhaps perpetual) medication.

So for now the biologics remain the most effective tool for inducing remission that we currently have.

Crohn's really is the wonder of the century. We know it's bacterial but we don't treat it like a bacteria. We know additives are not good for the gut but EEN (full of weird ingredients) is extremely effective for induction. It's almost like we don't know why all these treatments work but they just do. Mind boggling.

 

[Scipio]

Crohn's really is the wonder of the century. We know it's bacterial but we don't treat it like a bacteria. We know additives are not good for the gut but EEN (full of weird ingredients) is extremely effective for induction. It's almost like we don't know why all these treatments work but they just do. Mind boggling.

We don't treat it like a bacteria because treating it like a bacteria hasn't worked very well. At some point a theory, however attractive or logical, has to give way to actual results. When antibacterial therapy starts working as well as biologics do in restoring a semblance of a Crohn's-free life, and assuming the side effects and risks are no worse, I'll be the first in line to make the switch.

 

[asadmom]

We don't treat it like a bacteria because treating it like a bacteria hasn't worked very well. At some point a theory, however attractive or logical, has to give way to actual results. When antibacterial therapy starts working as well as biologics do in restoring a semblance of a Crohn's-free life, and assuming the side effects and risks are no worse, I'll be the first in line to make the switch.

Well said, as always.

 

[Ignotius]

to me i feel many tests fail by trying to treat it singularly......i understand it is "impractical" to enact more complicated trials, but its got to be a combination of diet and bacterial balancing etc which actually makes sense...rather than simply observing oddities in a one factor test, that will fail every time imho....we may get some power options one day too, but i dont think i could ever trust a simple cure for something like this...

 

[onolox]

Crohn's really is the wonder of the century. We know it's bacterial but we don't treat it like a bacteria. We know additives are not good for the gut but EEN (full of weird ingredients) is extremely effective for induction. It's almost like we don't know why all these treatments work but they just do. Mind boggling.

Full of weird ingredients? lol study more

 

[Ignotius]

Full of weird ingredients? lol study more

yeah actually they are.....literally any that ive looked at anyway.....artificial sweeteners etc......
i think she studies a pretty good ammt, theres alot of posts shes made thats helped me anyway i know that.

 

[onolox]

The ingredients are just basic things, not 'weird stuff'.
Maltodextrin, whey. vitamins...

 

[Ignotius]

try asking google simply something like maltodextrin + crohns.....its weird to consider that as an ingredient....or anything which is a known antagonizer...
"vitamins" can tend to not be "natural" as well which can predictably complicate issues vs a more direct form of nutrition.

ive shifted more to things like superfoods and moringa etc type things trying to phase mine out, but i still take 1/3 of one per day

 

[onolox]

https://link.springer.com/article/10.1007/s00394-019-02161-8
" While maltodextrin and the aspartame-based sweetener influenced the gut microbiome composition and production of SCFA, they did not induce dysbiosis and their effect might be considered favourable by inhibiting the growth of E. coli, thus promoting Bifidobacterium and correspondingly increasing the production of acetic acid and propionic acid. "

My hypothesis based on this study is that malto is promoted as bad because they don't analise it separately but this is only one study.
In an EEN malto or any other thing is absorbed so fast and travels so litthe that it can't make any difference in the gut.

 

[kiny]

The oral cavity is the only other area with high bacterial load, and not surprisingly people with crohn's disease frequently develop aphthous ulcers in their mouth.

A bit more evidence that the oral cavity in crohn's disease patients might serve as a bacterial reservoir for Klebsiella. The idea that the oral cavity in crohn's disease patients might chronicially reinfect patients is a something that has only be suggested a few times, but because aphthous ulcers are so common during active phases of crohn's disease, and because we know Klebsiella is involved in Crohn's disease, it is certainly a suggestion that deserves being studied.

"The Oral Microbiome in Treatment-Naïve Paediatric IBD Patients Exhibits Dysbiosis Related to Disease Severity that Resolves Following Therapy.

Analysis of community structure of the microbiome in tongue samples revealed that IBD samples diverged significantly from healthy control samples and exhibited a reduced abundance of Clostridia in addition to several major oral genera with an increased abundance of streptococci. This dysbiosis was more marked in patients with severe disease. Higher levels of the potential pathobionts Klebsiella and Pseudomonas spp. were also associated with IBD."

https://academic.oup.com/ecco-jcc/advance-article/doi/10.1093/ecco-jcc/jjac155/6761098?login=false

 

[kiny]

try asking google simply something like maltodextrin + crohns.....its weird to consider that as an ingredient....or anything which is a known antagonizer..."vitamins" can tend to not be "natural" as well which can predictably complicate issues vs a more direct form of nutrition.

ive shifted more to things like superfoods and moringa etc type things trying to phase mine out, but i still take 1/3 of one per day

EN are abundant in maltodextrin and they're all pretty much the same substance in every EN, with only slight variations depending on the time of hydrolysis used to make them. In Europe they are called glucose syrups.

There have been a few studies that suggested maltodextrin would promote the expansion of pathogenic species. But what these studies designed around a petri dish show, is not at all what we see in people with crohn's disease consuming maltodextrins through EN. Studies now consistently show that both adults and children with crohn's disease using EN show a rapid decrease in inflammation and decrease in bacterial load.

Maltodextrin is incredibly bioavailable and taken up rapidly by the upper intestine. I do not believe much of the maltodextrin consumed through EN is available to bacteria in the ileum or colon, if any. EN rapidly decreases bacterial load in both SIBO and Crohn's.

 

[asadmom]

EN are abundant in maltodextrin and they're all pretty much the same substance in every EN, with only slight variations depending on the time of hydrolysis used to make them. In Europe they are called glucose syrups.

There have been a few studies that suggested maltodextrin would promote the expansion of pathogenic species. But what these studies designed around a petri dish show, is not at all what we see in people with crohn's disease consuming maltodextrins through EN. Studies now consistently show that both adults and children with crohn's disease using EN show a rapid decrease in inflammation and decrease in bacterial load.

Maltodextrin is incredibly bioavailable and taken up rapidly by the upper intestine. I do not believe much of the maltodextrin consumed through EN is available to bacteria in the ileum or colon, if any. EN rapidly decreases bacterial load in both SIBO and Crohn's.

Can we achieve the same ie low inflammation and bacteria load with broth? Can EEN or PEN using broth be just as effective?

 

[asadmom]

A bit more evidence that the oral cavity in crohn's disease patients might serve as a bacterial reservoir for Klebsiella. The idea that the oral cavity in crohn's disease patients might chronicially reinfect patients is a something that has only be suggested a few times, but because aphthous ulcers are so common during active phases of crohn's disease, and because we know Klebsiella is involved in Crohn's disease, it is certainly a suggestion that deserves being studied.

If Klevbiella is known to be the/a culprit, why can't the doctors prescribe antibiotics for it? Or they can't be completely eliminated by the med we have now?

 

[asadmom]

I also wonder about fasting. Could some form of fasting achieve the same as EEN? No food, no bacteria load and 100% gut rest.

 

[kiny]

I also wonder about fasting. Could some form of fasting achieve the same as EEN? No food, no bacteria load and 100% gut rest.

Pathogenic bacteria involved in crohn's disease, especially Klebsiella, sustain nutrient deprivation for much longer than any other bacteria, both in the mouth and intestine. I don't think fasting would be that helpful.

The small intestine is also in need of daily nutrients to function properly, it is highly dependent on glutamine to maintain its barrier function to keep out bacteria.

 

[asadmom]

Pathogenic bacteria involved in crohn's disease, especially Klebsiella, sustain nutrient deprivation for much longer than any other bacteria, both in the mouth and intestine. I don't think fasting would be that helpful.

The small intestine is also in need of daily nutrients to function properly, it is highly dependent on glutamine to maintain its barrier function to keep out bacteria.

So I guess EEN can achieve the starvation? BTW, is glutamine the same as l-glutamine powder that you can buy over the shelf?

 

[kiny]

If Klevbiella is known to be the/a culprit, why can't the doctors prescribe antibiotics for it? Or they can't be completely eliminated by the med we have now?

We have in a way right. The bacteria involved in Crohn's disease are all enterobacteriaceae, and the most effective antibiotic in Crohn's is cipro, which is very effective against gram negative enterobacteriaceae.

It's just that these antibiotics will run into resistant bacteria, and there are limits to how long you can treat someone with a fluoroquinolone before you can no longer justify the risk of serious side effects. You can treat a person with cipro for a few weeks, it's harder to justify putting someone on cipro for months, knowing you might be creating resistant strains that might no longer be susceptible when we do find a targeted approach.

But if a person with crohn's disease is completely unresponsive to traditional treatment, yes cipro should be used to treat them.

 

[Ignotius]

yes i think its a little of a trigger for me haha its like is it not possible to just not use things found to be harmful?....i saw another study like oh they need oil lets try feeding them corn and see what happens.......this is doctors and educated intelligent people....it almost feels like we arent trying at times.

i know the fiber is a trick situation, but there is alot that can be done here with optimal ingredients and special preparation techs.....they want to make a half an effort then call it a fail, im not impressed.....im not running to artificial ingredients tho, i dont see how that could make sense, its seems like a well a little bit of poison is ok type idea......sure some of these forumulas work impressively in some trials but could it be better effective? and scaled into actual more semi solid type introductions etc i gotta feel like thats absolutely yes.....im not a scientist tho just trying to listen to my body and common sense.

 

[kiny]

BTW, is glutamine the same as l-glutamine powder that you can buy over the shelf?

When people mention glutamine yes, they mean L-glutamine, D-glutamine has no nutritional function.

We have tried giving people with crohn's disease extra glutamine several times, it has no effect since most people with crohn's disease aren't short on glutamine.

But if you would start fasting, or if a person with crohn's disease hasn't eaten in days, they would certainly benefit from consuming enough proteins, it doesn't have to be L-glutamine supplements specifically.

 

[asadmom]

So good to learn something new here! So @kiny can you please share with us what you have discovered about anything Crohn's since last time you visited here?

 

[kiny]

The aphthous ulcers in the mouth of crohn's patients interest me since I had many myself and they're understudied in patients. Oral bacteria and the bacteria found in the intestine in patients with crohn's disease are intertwined in some way, especially for bacteria like Klebsiella. If there is a direct link, we could take oral samples and biopsies to follow disease progression and find targeted approaches to treating patients.

 

[Ignotius]

i like to think things like epicor that increase immunoglobin-A might make a difference in helping prevent unusual expressions/imbalances... or correcting them.....but i dont think it can only rely on things like that so simply for everyone.......if enough pieces of a puzzle are put together tho it makes a clearer picture....

i am pretty interested how they will target imbalances in the near future....it kind of feels like general probiotics are sloppy and sometimes actually harmful but i understand they may be able to target things more specifically with unique phages or however thats better targeted vs nuclear antibiotics.......i keep noticing new things all the time tho like probiotic suppositories? maybe it helps better going in the other end idk, theres alot of data we need but the better the studies are put together i know.....its a little confusing why that seems so hard to do sometimes tho

 

[Ignotius]

but of course if there are active issues going on the best treatment can make things worse.....it seems like there needs to be several step treatments for changeups when things progress its just alot to figure out for anyone i guess

 

[asadmom]

@kiny something that really puzzles me is I've heard of a case where the patients labs are all normal and one day out of the blue was hospitalized for partial obstruction. How is it that there is no sign of inflammation but the bowel wall manages to "thicken"? The converse is also very interesting in this case where a patient is in deep remission but has many symptoms? So do we just explain these away by "Crohn's is complicated"?

 

[asadmom]

The aphthous ulcers in the mouth of crohn's patients interest me since I had many myself and they're understudied in patients. Oral bacteria and the bacteria found in the intestine in patients with crohn's disease are intertwined in some way, especially for bacteria like Klebsiella. If there is a direct link, we could take oral samples and biopsies to follow disease progression and find targeted approaches to treating patients.

You should run a study!

 

[onolox]

The aphthous ulcers in the mouth of crohn's patients interest me since I had many myself and they're understudied in patients. Oral bacteria and the bacteria found in the intestine in patients with crohn's disease are intertwined in some way, especially for bacteria like Klebsiella. If there is a direct link, we could take oral samples and biopsies to follow disease progression and find targeted approaches to treating patients.

And about the appendix? It stores bacteria...

 

[JackG]

@Pangolin Thanks - I've done some elimination diets but nothing really stood out. For me, finding key foods that trouble me are tough. Ugh.

I have had Crohn's for 40 years last April; it started with misdiagnosis and an emergency ileostomy. At this point all dairy, chocolate and dark liquids are my triggers. 10 years ago Humira worked for me, but it gave me terrible psoriasis. Switched to Entyvio and it works without the skin issues. I take a probiotic called PB8 everyday and i think that's a miracle help.
I cheat and add non dairy creamer to coffee, eat a rare candy bar or a little ice cream, but my system always knows. Taking an Imodium once a week or so helps enable my coffee habit.

 

[ncman]

@kiny something that really puzzles me is I've heard of a case where the patients labs are all normal and one day out of the blue was hospitalized for partial obstruction. How is it that there is no sign of inflammation but the bowel wall manages to "thicken"? The converse is also very interesting in this case where a patient is in deep remission but has many symptoms? So do we just explain these away by "Crohn's is complicated"?

My take on this is that there are a few scenarios where this could apply - the first would be patients on immunosuppressive medication.

Because while the medication is 'blocking' the immune system, the underlying problem of CD (i.e. the infiltration of bacteria into the intestinal wall) remains - and the medication is doing nothing to address the underlying problem, just making symptoms disappear. As summarised in AW Segal's 2016 paper:

Immunosuppressant treatment further compromises the underlying innate immune deficit to mucosal damage, thereby increasing the like-
lihood of further infection and the influx of bowel contents into the tissues, possibly converting CD from a sporadic to a chronic condition.

So while the patient is well, inflammatory markers are low, the medication is effectively making the problem of CD worse.

There are a variety of reasons why immunosuppresives stop working (e.g. the body starts building antibodies to the medication - there are many more reasons which I haven't listed), ultimately while it might have offered relief from the symptoms of CD for some time (6 months, 1 year, 25 years plus for some patients), but at some point it will become less effective at blocking the immune system.

The intestinal wall is still full of the bacteria that hasn't been cleared - and the body in its infinite wisdom must find a way to do this - and it will do it quickly.

Other scenarios which I think this would possibly apply is to sites of surgical anastamosis (as there is a 90%+ chance of CD recurrence).

And also if you have had low-grade chronic inflammation for some time - although I'm not clear why as if you are keeping the bacterial load low, why would the body see the need to clear more aggressively.

 

[asadmom]

My take on this is that there are a few scenarios where this could apply - the first would be patients on immunosuppressive medication.

Because while the medication is 'blocking' the immune system, the underlying problem of CD (i.e. the infiltration of bacteria into the intestinal wall) remains - and the medication is doing nothing to address the underlying problem, just making symptoms disappear. As summarised in AW Segal's 2016 paper:

Immunosuppressant treatment further compromises the underlying innate immune deficit to mucosal damage, thereby increasing the like-
lihood of further infection and the influx of bowel contents into the tissues, possibly converting CD from a sporadic to a chronic condition.

So while the patient is well, inflammatory markers are low, the medication is effectively making the problem of CD worse.

There are a variety of reasons why immunosuppresives stop working (e.g. the body starts building antibodies to the medication - there are many more reasons which I haven't listed), ultimately while it might have offered relief from the symptoms of CD for some time (6 months, 1 year, 25 years plus for some patients), but at some point it will become less effective at blocking the immune system.

The intestinal wall is still full of the bacteria that hasn't been cleared - and the body in its infinite wisdom must find a way to do this - and it will do it quickly.

Other scenarios which I think this would possibly apply is to sites of surgical anastamosis (as there is a 90%+ chance of CD recurrence).

And also if you have had low-grade chronic inflammation for some time - although I'm not clear why as if you are keeping the bacterial load low, why would the body see the need to clear more aggressively.

They are not on any medication actually. One is trying the diet and all tests normal for a few years and all of a sudden landed in ER for partial obstruction. One got side effects from antiTNF so dropped the drug but over time experiencing symptoms but all tests normal. Could you think of other reasons that might explain these odd cases?

Totally agreeing to your point about ignoring the underlying causes! I also find it odd that we treat the surface, short the circuit but ignore the real problem yet at the same time many patients do extremely well by being treated this way. I mean this is the therapy protocol we use at the moment and the evidence overwhelmingly shows that Crohn's can be managed this way.

 

[ncman]

It is unusual - I guess your case then links into my third scenario, where if the diet was keeping the bacterial load low, why would the body need to enact drastic 'cleaning' measures - I don't know, maybe someone else can shed some light.

Calprotectin has always been an accurate marker for me - I was just reading another thread on here where someone said calpro and albumin were the main ones to track...'the trend is your friend'.

As an aside, the forum is so quiet these days - any idea where everyone has gone? I used to go here, and Healing Well, and Reddit /r/ibd and /crohnsdisease - but the forums are so quiet, and Reddit is 'too noisy'. I've joined one or two plant based Facebook groups, but they tend to promote only 'one view'.

 

[asadmom]

It is unusual - I guess your case then links into my third scenario, where if the diet was keeping the bacterial load low, why would the body need to enact drastic 'cleaning' measures - I don't know, maybe someone else can shed some light.

Calprotectin has always been an accurate marker for me - I was just reading another thread on here where someone said calpro and albumin were the main ones to track...'the trend is your friend'.

As an aside, the forum is so quiet these days - any idea where everyone has gone? I used to go here, and Healing Well, and Reddit /r/ibd and /crohnsdisease - but the forums are so quiet, and Reddit is 'too noisy'. I've joined one or two plant based Facebook groups, but they tend to promote only 'one view'.

Yeah the plant based ones are not helpful if you are looking to learn or meet people who are more open-minded. They are more like a echo chamber, reinforcing the same idea and same practice or experience from 10 years ago. I prefer SCD and MAP. Love Ray Peat's

 

[momsa]

I was reading all of these messages talking about the theory of a bacterial cause of Crohn's, and I thought it was interesting in light of my twin's situation. I have identical twins whose symptoms of Crohns started at the same time, the beginning of college. Both have disease restricted to the colon (mainly sigmoid). Before diagnosis, when one of my twins became quite acutely ill (my twins' symptoms when they flare have mainly been fever and lack of appetite, though there was diarrhea at this point too) the PCP gave my one son a course of flagyl. There was a dramatic improvement. He turned around within a week - he ate again, the bloody diarrhea disappeared, fever went away. Nothing given to either of my sons since that time has shown at all such a dramatic improvement. The son who was given the flagyl is now doing well, the other son isn't doing as well. When I tell this to doctor after doctor, they just scratch their heads.

 

[asadmom]

I was reading all of these messages talking about the theory of a bacterial cause of Crohn's, and I thought it was interesting in light of my twin's situation. I have identical twins whose symptoms of Crohns started at the same time, the beginning of college. Both have disease restricted to the colon (mainly sigmoid). Before diagnosis, when one of my twins became quite acutely ill (my twins' symptoms when they flare have mainly been fever and lack of appetite, though there was diarrhea at this point too) the PCP gave my one son a course of flagyl. There was a dramatic improvement. He turned around within a week - he ate again, the bloody diarrhea disappeared, fever went away. Nothing given to either of my sons since that time has shown at all such a dramatic improvement. The son who was given the flagyl is now doing well, the other son isn't doing as well. When I tell this to doctor after doctor, they just scratch their heads.

Did your son not need any medication later to manage their Crohn's?

 

[momsa]

Sorry, I wasn't clear. He was put on Stelara. The assumption is that he would be worse now if he weren't on it.

 

[asadmom]

Sorry, I wasn't clear. He was put on Stelara. The assumption is that he would be worse now if he weren't on it.

It's an amazing insight. Thank you for sharing. I just didn't know enough... My son's diagnosis really caught me off guard. If I was more knowledgeable back then I would for sure try more things before jumping on the med.

 

[momsa]

I don't regret using biologics, I just wonder about the role of antibiotics. I know it's complicated, because you don't want the wrong bacteria to grow. It's just that I was amazed that the flagyl seemed to cause what was by far a more dramatic change than anything else.

 

[braveheart]

I think the origin of all auto-inmune diseases, including Crohn and Ulcerative Colitis is genetic. Of course there may be some bacteria that triggers the disease but that does not mean the bacteria is the culprit. Consider lots of healthy people are exposed to that bacteria and they do not develop IBD. Notice Momsa explained her twins were diagnosed with Crohn at the same time when they started college, but I bet no other students in that college developed CD.

Moreover, if you check specifications, Humira also works for arthritis, Stelara also works for psoriasis. All auto-inmune diseases seems to be related.

I know antibiotics and steroids are effective treatments for CD as same as inmunosuppressants or biologics but I still think the problem is genetic. I know a particular case does not make the rule, but my father and grandpa had arthritis, as same as my sister has. My son and I have Crohn disease. I can't help thinking of Crohn and all auto-inmune diseases as something genetic.

 

[momsa]

Agreed on the genetic component. To be clear, my twins started getting symptoms just slightly before they went to college, when they were on a trip to the middle east.
Now what I wonder is to what degree response to treatment is genetic. In other words, can I glean something about what medicines one twin will respond to from the responses to medications of the other twin?

 

[Pangolin]

Crohn's is not an autoimmune disease. It's an immune-mediated disease, but there's no evidence that it's an immune reaction against the self. It appears to be an immune reaction against non-self molecules such as bacteria, yeast, and possibly foods.

 

[my little penguin]

I have seen it argued autoimmune for years
However the latest I have seen is auto inflammatory type of disease which is different than auto immune
https://pubmed.ncbi.nlm.nih.gov/31084224/
https://www.verywellhealth.com/is-crohns-autoimmune-5188106
https://www.sciencedirect.com/topics/immunology-and-microbiology/autoinflammatory-syndromes

 

[wduk]

Is there much strong evidence regarding over sterilised environments so we are less exposed to bacteria to make our gut more resilient.

I recall reading crohn's disease rates increase as developing nations increased in hygiene standards directly related to education and wealth. But never saw much beyond that to know how strong the correlation was or whether there was a causation.