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microbiome, leaky gut remedies beat crohns and RA

here's my story -- and my mission

got crohns, suffered for several years, then SEVERE inflammatory arthritis. bed ridden and in severe pain with several major joints swollen and red. went to rheumatologist, blood work a horror story. she puts me on high dose prednisone to get things under control. that worked great for the pain of RA. i was hooked on prednisone. but the crohns stuff continued.

she urges me to get on some other med. i dont want to. begin study to find the cause of RA. stay on prednisone for months while doing my research and trying every supplement known to man. stumble onto some evidence about the gut microbiome and leaky gut. give it a shot.

took about 3 months - tapering off of the prednisone - and turning my gut health around -- microbiome protocol and leaky gut protocol. both crohns and RA completely disappeared. my rheumy was stunned. i told her a brief outline of how i did it. she took notes. hope she's using it for her patients now.

typing this about 2 years after putting both of those autoimmunes to bed. no sign or symptoms of them. i've gone from unable to walk to playing basketball again. it's taken some time rebuilding the connective tissue that was shredded by the RA. but steady progress....

my mission --- to spread this information around to all autoimmune sufferers. just about all of them have the same root cause(s). namely the two listed above. this is my first post of many (i hope). i will field all questions. the only reason i'm here is to help. i feel like it is my calling and i am doing my duty.

i have used these protocols to heal friends and family of other issues -- anxiety/panic attacks, psoriasis, vertigo, lactose intolerance, etc

i have a ton of scientific studies/trials about this topic. you can imagine, i study this stuff daily, going on 4 years now :)

microbiome science is an emerging miracle. the things that are coming are mind blowing.

i'll stop here for now.

best regards

edit -- i plan on mainly working in the crohns research subforum. find me there posting the science/theory of reversing crohns by working on the gut microbiome and repairing leaky gut. imo these two issues are the cause of the majority of chronic diseases
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my little penguin

Staff member
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crohns can have extra intestinal manifestations
Including arthritis
In this case it’s not RA
It’s based on crohns
Some have activity with arthritis regardless of crohns activity
Others only have arthritis when the inflammation in the gut is active
Which means as long as the crohns is quiet the arthritis is quiet
thanks for the info! from your link -- this is exactly how it went down - leaky gut letting food/bacteria into my bloodstream

Some researchers believe that the long-lasting inflammation found in the intestines of people with IBD damages the bowel, which in turn may allow bacteria to enter the damaged bowel wall and circulate through the blood stream. The body’s reaction to these bacteria may cause other problems, including inflammation in the joints and/or spine, skin sores, and inflammation of the eyes.

my little penguin

Staff member
Thirteen years at this
Crohns and juvenile arthritis in my kiddo
Glad your diet work for you
Diet modifications have worked for some
Not all
But some
Definitely not my kiddo -we tried it all
Only een worked for crohns
His arthritis is independent of crohns activity.
Just be sure to get regular bloodwork
Imaging (MRE) and scopes
Since symptoms on the outside don’t always reflect what is going on inside
give me a shot at at. i would LOVE to throw all of my weight into helping the kiddo. i'll unleash it all, maybe something in there will interest you. where should i do it?
extensive paper. grabbed some pertinent clips. my bold

Leaky Gut in IBD: Intestinal Barrier–Gut Microbiota Interaction

Destruction of the intestinal barrier is referred to as developing a “leaky gut,” which causes a series of changes relating to the occurrence of IBD. Changes in the interactions between the intestinal barrier and gut microbiota are particularly crucial in the development of IBD.

The gut microbiota can protect against the development of IBD, suggesting that regulation of the gut microbiota could also be a future treatment option. IBD patients often exhibit dysbiosis, as confirmed by the results from fecal and mucosal microbial analyses. Intestinal dysbiosis and IBD are often mutually causal and persistent dysbiosis leads to long-standing and severe inflammation. However, some commensal bacteria improve IBD and may be a future treatment option.

A breached intestinal barrier allows microbes unlimited access to the lamina propria and the bloodstream [4], a condition referred to as “leaky gut.” IBD patients often suffer from abnormal intestinal permeability and enteric blood barrier impairment [5]. Destruction of the intestinal barrier is one characteristic of IBD

Fecal microbial richness is an average of 25% lower in IBD patients than in healthy people [11]. In fecal samples from patients with IBD, Bacteroidetes, Proteobacteria, Enterobacteriaceae family [12], Fusobacterium, - and Enterococcus faecalis [13] are significantly increased, while Bifidobacteria and butyrate-producing bacteria such as Faecalibacterium, Eubacterium, Roseburia, Lachnospiraceae and Ruminococcaceae are decreased compared with healthy individuals [14, 15]. Actinobacteria and Tenericutes are decreased in CD patients, and Firmicutes is decreased in UC patients compared with healthy individuals. Roseburia intestinalis (R. intestinalis), which is abundant in the intestine and enables the production butyrate, is decreased in IBD patients compared with healthy individuals, and is related to a higher number of IBD risk alleles

Intestinal inflammation promotes the proliferation of fungi, which can in turn regulate intestinal inflammation. Candida albicans (C. albicans) plays a pro-inflammatory role and aggravates the development of IBD. Lactobacillus rhamnosus L34 antagonizes C. albicans and alleviates IBD severity by reducing intestinal barrier damage, ameliorating intestinal and systemic inflammation, and improving dysbiosis [30]. Probiotics such as Lactobacillus reuteri ATCC 55730, Bifidobacterium triple viable agents, or a multi-strain probiotic combined with conventional IBD drugs such as glucocorticoid and mesalazine show a greater ability than monotherapy to alleviate inflammatory responses, upregulate the expression of intestinal barrier-related proteins, and promote mucosal homeostasis [31-34]. Bifidobacterium adolescentis was shown to reinforce the intestinal barrier by enhancing mucus thickness and increasing occludin, Muc2, and Muc3 mRNA expression in a mouse model of chronic colitis

Dietary fiber serves as an energy source for intestinal bacteria. In a fiber-free diet condition, Muc2 polysaccharides are consumed by bacteria, resulting in thinning of the inner mucous layer [45] and bacterial invasion into the lamina propria, which ultimately promotes IBD development

Abnormal intestinal permeability precedes the onset of CD by 3 years
and may be an important component of pathogenesis. Increased intestinal permeability in asymptomatic individuals is significantly associated with the risk of developing CD

IBD-related dysbiosis may lead to bile acid dysmetabolism and affect intestinal homeostasis [105]. Ursodeoxycholic acid (UDCA), a component of bear bile, is cytoprotective and anti-inflammatory. Administration of UDCA inhibits excessive apoptosis and abnormal increases in epithelial permeability, maintaining barrier function and protecting against intestinal inflammation

Short-chain fatty acids (SCFAs) are mainly produced in the cecum and the proximal colon by Bacteroidetes and Firmicutes. A decrease in intestinal SCFAs may result in increased intestinal permeability and severe inflammation [111]. Gut microbiota-derived butyrate maintains the epithelial barrier by inhibiting phosphorylation of AKT and NF-κB p65 signaling pathway in macrophages [112]. Butyrate promotes epithelial barrier function by activating transcription factors such as STAT3 and SP1 and inducing genes encoding tight junction and protein reassembly.

Regarding the mechanical barrier, tight junction dysregulation is associated with chronic inflammation, and abnormal intestinal permeability precedes the onset of disease.

However, mucin expression gradually increases when patients are in remission. Therefore, changes in the intestinal barrier affect all stages of IBD.

Changes in the interplay between the intestinal barrier and the gut microbiota are particularly crucial for IBD.
large study shows leaky gut precedes crohns. the same could be said for the great majority of chronic diseases, especially autoimmunes

GEM Study Links Leaky Gut to Crohn’s Disease

This is the first report of pre-existing abnormal barrier function in a large study of healthy individuals followed over time for the development of Crohn’s disease demonstrating that the LacMan ratio can predict disease.
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