Early exposure to antibiotics decreases risk of developing crohn's disease.

[kiny]

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[kiny]

The 2022 Danish study found a negligeable risk associated with exposure to antibiotics, this study found exposure to antibiotics actually conferred a protective effect.

The theory that exposure to antibiotics, leads to dysbiosis, subsequent crohn's disease, and can be corrected with probiotics or fecal plants, is such a ridiculous theory. Hopefully it goes into the trash if another large study finds no association. Any associations are likely just a reflection of socioeconomic status. These same studies often find high socioeconomic status is associated with high prevalence of CD among their population, and somehow don't make the link that people with access to healthcare are people of higher socioeconomic status, readily available access to antibiotics and are far more likely to seek out healthcare professionals and end up in your statistics.

However, exposure to foodborne infection and subsequent development of crohn's disease is supported by a lot of far more reliable data. Several of these studies have not been performed in the general population, but are records of servicemen with comparable socioeconomic status and similar access to healthcare.

 

[Scipio]

Interesting. Although in my own trial of n=1, having received massive doses of penicillin at ages 4 and 5 to treat suspected rheumatic fever, did not prevent my developing Crohn's disease in middle age.

 

[J100]

It is interesting read. It is a long read and I couldn't figure out the efficacy and what other control parameters were there. Assuming that this is one singular factor and what the study states is true, then this settles the debate that gut microbiome dysbiosis is the cause of Crohn's disease. But I wouldn't put too much weight into this study by itself because as we all know that CD is a complex disease with perhaps multiple causes and unless there is a study which can figure out those multiple factors then we can't reach a conclusion. And the fact of the matter is that any trial which is conducted, there is only one parameter which is varied not multiple, therefore doing a study will be extremely hard. My gut feel is that there is something in the environment which triggers it.

 

[kiny]

I think it is possible ileal crohn's disease has just a simple singular cause. Yes, only some people have penetrating disease (fistula), only some people have strictures, only some have granuloma, only some have creeping fat. But at the end of the day, diverting the fecal stream in Rutgeerts his studies caused resolution of inflammation in all patients, EN causes resolution of inflammation in the overwhelming majority of patients with ileal disease.

But crohn's that is restricted to the colon, seems very different. Crohn’s disease restricted to the colon was not too long ago just considered to be UC. Burrill Crohn and Oppenheimer, described crohn's disease as regional ileitis, Dalziel described it as enteritis, inflammation without ileal involvement was simply not considered crohn's disease. More proximal inflammation was also not considered crohn's disease. Crohn's disease was exclusively used for inflammation of the ileum.

This is the first sentence in the study where Burrill Crohn and Oppenheimer are the first to describe crohn's disease, referring to a 1932 study about regional enteritis: "We propose to describe, in its pathologic and clinical details, a disease of the terminal ileum. The terminal ileum is alone involved." There's no mention of the colon, no mention of any other part in the GI tract.

When some say: "Crohn's disease can happen anywhere in the digestive tract". I call it silly, becasue Burrill Crohn would have strongly objected to that description, it makes no sense, I don't know who made up that ridiculous notion, there's no crohn's disease of the stomach. You need a new GI if a GI says you have crohn's disease in your stomach.

I don't understand colonic disease, I have been less interested in it because I have only crohn's in the ileum, but it is not just that, it is also because the colon is a pretty simple organ compared to the ileum which means many ileal studies do not translate to colonic disease. The colon doesn't have peyer's patches, no M cells, there's no paneth cells, it has a fraction of the TLRs the ileum has, it doesn't take up nutrients, response to EN is worse, the colon is absolutely nothing like the ileum. What the colon does have is a much larger population of commensal bacteria.

One of the reasons I keep objecting and am so apprehensive about the idea that dysbios causes crohn's disease, is simply because that would imply massive inflammation in the colon, the colon where the large majority of commensal bacteria reside. Because unless you're using a biopsy sample, you're measuring colonic populations, not ileal. But most people with ileal disease have either never had colonic inflammation, or have had little to no colonic involvement.

I have no explanation for crohn's in the colon, just like I can't come up with any explanation for UC.

 

[kiny]

Even if different bacteria or fungi are involved in each patient, the cause of chronic relapsing inflammation would still be the same. Chronic insult from pathogens and the inability of crohn's disease patients to clear them. The intestine gets overwhelmed, macrophage penetrating pathogens entering through M cells and genetic predisposition would leave the permeable ileum exposed. Large numbers of macrophages in the lamina propria and migration of neutrophils would result in inflammation, but without resolve. Bowel rest, use of EN, IV feeding, would lower the fecal stream and bacterial insult of the ileum.

The pathogens might be different, but the disease description would be the same.