gut dysbiosis/leaky gut the universal disease cause?

Crohn's Disease Forum

Help Support Crohn's Disease Forum:

C

cheka

Joined
Mar 31, 2024
Messages
219
all of these came out within the last month. gut dysbiosis as a universal cause for many diseases. the mysteries of disease are being unraveled. the future is bright!

https://pubmed.ncbi.nlm.nih.gov/33166939/
Mounting evidence has suggested gut microbial imbalance (dysbiosis) as a core pathophysiology in the development of GI motility and metabolic disorders, such as irritable bowel syndrome and diabetes.

https://pubmed.ncbi.nlm.nih.gov/30535609/
Studies in animal models and humans have shown that a persistent imbalance of gut's microbial community, named dysbiosis, relates to inflammatory bowel diseases (IBD), irritable bowel syndrome (IBS), diabetes, obesity, cancer, cardiovascular and central nervous system disorders.

https://pubmed.ncbi.nlm.nih.gov/38527589/
Leukemia are a set of clonal hematopoietic malignant diseases which develop in the bone marrow. Several factors influence its development and progression. Among these, the gut microbiota is a major factor influencing a wide array of its processes.

https://pubmed.ncbi.nlm.nih.gov/38540258/
In recent years, growing evidence has pointed to the critical involvement of the pancreas in regulating the intestinal microbiota, as well as the impact of the intestinal microbiota on pancreatic physiology, which implies the existence of a bidirectional connection known as the "gut-pancreas axis". It is theorized that any change at either of these levels triggers a response in the other component, hence leading to the evolution of pancreatitis.
 
This is a more impressive study, and some researchers have written articles specifically commenting on it.
https://www.gastrojournal.org/article/S0016-5085(23)00805-3/pdf
Gut dysbiosis in Crohn's disease: Never so close to solving the chicken-and-egg enigma: Commentary to "Gut microbiome composition is associated with future onset of Crohn's disease in healthy first-degree relatives, by Raygoza Garay JA et al., Gastroenterology 2023"
https://pubmed.ncbi.nlm.nih.gov/38145785/
How exciting it is!
But we need to konw why the gut dysbiosis happened and what is the real trigger.
 
dysbiosis comes from what we put in our mouths and swallow. thankfully the fix is the same thing - what we put in our mouths

posted my story in the introduction subforum -- crohns and SEVERE inflammatory arthritis symptoms went poof when i went on protocols to fix dysbiosis and leaky gut. have to work on both. i then moved on to healing everybody around me of their issues. now taking the show on the road, that's why i'm here -- to try to help humanity, esp suffering humanity, get better

i see posters that have been here for many years, still suffering. to them i say -- give this a shot - it's the real deal! also help those around you that are suffering

nothing in the repair protocols are nearly as risky as the pill poisons. if you have the courage to take that stuff, you have 100x the courage to change the things going in the mouth
 
Last edited:
longzhiwu said:
This is a more impressive study, and some researchers have written articles specifically commenting on it.
https://www.gastrojournal.org/article/S0016-5085(23)00805-3/pdf
Gut dysbiosis in Crohn's disease: Never so close to solving the chicken-and-egg enigma: Commentary to "Gut microbiome composition is associated with future onset of Crohn's disease in healthy first-degree relatives, by Raygoza Garay JA et al., Gastroenterology 2023"
https://pubmed.ncbi.nlm.nih.gov/38145785/
How exciting it is!
But we need to konw why the gut dysbiosis happened and what is the real trigger.
Click to expand...

thanks for the links! you and could fill up this forum with all of the diseases that gut dysbiosis/leaky gut cause. pages and pages of different diseases all linked to same cause. this is GREAT news -- making the diseases disappear, or preventing them, is roughly the same protocols. crohns also features sibo -- so one extra step. still not complicated, and totally within our powers -- we need not cede our authority to a paid pill dispenser. dispensers main play is to block this or that, chasing symptoms around. these gut healing protocols get to the source - and make things disappear completely, forever
 
they are figuring it out. twins case shows not genetic, but epigenetic (prone to)

https://www.mdpi.com/1422-0067/24/4/3817
2. Gut Microbiota and IBD

Currently, in Europe and the United States, 3.6 million people suffer from IBD, including UC and CD, which are becoming increasingly prevalent worldwide [29]. IBD is an autoimmune disease involving intestinal inflammation; however, it has garnered attention due to the crosstalk between the gut microbiota and autoimmune systems. The gut microbiota has been shown to trigger IBD-initiating events. The composition of the gut microbiota is different between healthy participants and IBD patients [30]. The use of antibiotics also leads to the onset of IBD due to the alteration of the composition and function of the gut microbiota [31].

The interaction between the gut microbiota and host plays a critical role in maintaining the function of the host’s immune system [32]. Changing environmental events such as the overuse of antibiotics and changes in diet may enhance autoimmune and inflammatory disorders by modulating the gut microbiota composition, leading to dysbiosis [33]. Thus, a crucial relationship exists between IBD and the microbial communities in the human gut. Although IBD is widely attributed to altered interactions between gut microbes and the intestinal immune system, the exact mechanism underlying gut microbiota dysfunction in IBD remains unclear [34]. Although the pathogenesis of IBD is unknown, the inflamed gastrointestinal tract in patients with IBD is a common feature of an imbalance (dysbiosis) in the gut microbiota. Recently, much evidence has been provided to show that gut dysbiosis leads to the disruption of immune tolerance, which may induce or exaggerate IBD [35].

Studies with human participants have clarified that the composition of the gut microbiota is different in patients with IBD compared with that in healthy subjects [30]. Additionally, the gut microbiota is different between patients with UC and CD [36]. Analyses of the gut microbiota in patients with IBD worldwide has led to the observation that dysbiosis involves an increase or decrease in specific intestinal bacterial species in patients with IBD. Morgan et al. reported that a large, long-term prospective cohort study showed that patients with IBD have characteristic gut microbiota compared with those in healthy participants [37].

The abundance of Roseburia and Phascolarctobacterium was significantly decreased, whereas that of Clostridium was increased in the gut microbiota of patients with UC or CD. Roseburia is associated with anti-inflammatory regulatory T cell production in the intestinal tract [38], and Phascolarctobacterium consumes only succinate and produces propionic acid when co-cultured with Paraprevotella [39]. Propionic acid is a short-chain fatty acid (SCFA) that has anti-inflammatory effects [40]. Patients with IBD have decreased SCFA-producing Phascolarctobacterium, suggesting that the anti-inflammatory effects of SCFAs might be reduced, which could consequently exacerbate IBD symptoms.

Generally, close relatives living in the same environment have similar gut microbiota, but a study in twins reported that when one twin pair was healthy and the other had IBD, the microbial compositions in the twins were different [43]. As this study included twins, it eliminated the influence of the genetic background on the abundance of F. prausnitzii and other specific genera such as Alistipes, Collinsella, and Ruminococcaceae. This result suggests that the onset of IBD might be more strongly influenced by environmental factors than by genetic factors, especially with regard to the gut microbiota, which were reduced in IBD patients compared to healthy subjects.

These results suggested that the onset of IBD might be more strongly influenced by environmental factors, especially gut microbiota, than by genetic factors. Moreover, a multi-omics analysis including metagenomic, metatranscriptomic, metabolomic, and other analyses revealed that the gut microbiota and their metabolites in CD and UC were different during the active and remission phases [44].
 
https://pubmed.ncbi.nlm.nih.gov/27548430/
The Search for Causative Environmental Factors in Inflammatory Bowel Disease

The best investigated environmental factor identified in IBD cohort analyses is smoking. Other environmental factors that have been associated with clinical presentation or risk of inflammatory flares as well as increased incidence are diet and food additives. The so-called 'hygiene hypothesis' suggests that increased hygiene in childhood associated with reduced exposure to pathogens may leave the mucosal immune system insufficiently trained and thus prone to uncontrolled inflammation.

Oral contraceptives and non-steroidal anti-inflammatory drugs are the 2 main classes of frequently taken drugs that have been attributed to have the potential to cause flares of the disease. What is likely to be the connection between the genetic susceptibility and the environmental triggers? There is broad evidence for a critical role of the commensal enteric microbiota as a modulator of immunologic responses relevant during onset and chronification of IBD.
 
cheka said:
they are figuring it out. twins case shows not genetic, but epigenetic (prone to)

https://www.mdpi.com/1422-0067/24/4/3817
2. Gut Microbiota and IBD

Currently, in Europe and the United States, 3.6 million people suffer from IBD, including UC and CD, which are becoming increasingly prevalent worldwide [29]. IBD is an autoimmune disease involving intestinal inflammation; however, it has garnered attention due to the crosstalk between the gut microbiota and autoimmune systems. The gut microbiota has been shown to trigger IBD-initiating events. The composition of the gut microbiota is different between healthy participants and IBD patients [30]. The use of antibiotics also leads to the onset of IBD due to the alteration of the composition and function of the gut microbiota [31].

The interaction between the gut microbiota and host plays a critical role in maintaining the function of the host’s immune system [32]. Changing environmental events such as the overuse of antibiotics and changes in diet may enhance autoimmune and inflammatory disorders by modulating the gut microbiota composition, leading to dysbiosis [33]. Thus, a crucial relationship exists between IBD and the microbial communities in the human gut. Although IBD is widely attributed to altered interactions between gut microbes and the intestinal immune system, the exact mechanism underlying gut microbiota dysfunction in IBD remains unclear [34]. Although the pathogenesis of IBD is unknown, the inflamed gastrointestinal tract in patients with IBD is a common feature of an imbalance (dysbiosis) in the gut microbiota. Recently, much evidence has been provided to show that gut dysbiosis leads to the disruption of immune tolerance, which may induce or exaggerate IBD [35].

Studies with human participants have clarified that the composition of the gut microbiota is different in patients with IBD compared with that in healthy subjects [30]. Additionally, the gut microbiota is different between patients with UC and CD [36]. Analyses of the gut microbiota in patients with IBD worldwide has led to the observation that dysbiosis involves an increase or decrease in specific intestinal bacterial species in patients with IBD. Morgan et al. reported that a large, long-term prospective cohort study showed that patients with IBD have characteristic gut microbiota compared with those in healthy participants [37].

The abundance of Roseburia and Phascolarctobacterium was significantly decreased, whereas that of Clostridium was increased in the gut microbiota of patients with UC or CD. Roseburia is associated with anti-inflammatory regulatory T cell production in the intestinal tract [38], and Phascolarctobacterium consumes only succinate and produces propionic acid when co-cultured with Paraprevotella [39]. Propionic acid is a short-chain fatty acid (SCFA) that has anti-inflammatory effects [40]. Patients with IBD have decreased SCFA-producing Phascolarctobacterium, suggesting that the anti-inflammatory effects of SCFAs might be reduced, which could consequently exacerbate IBD symptoms.

Generally, close relatives living in the same environment have similar gut microbiota, but a study in twins reported that when one twin pair was healthy and the other had IBD, the microbial compositions in the twins were different [43]. As this study included twins, it eliminated the influence of the genetic background on the abundance of F. prausnitzii and other specific genera such as Alistipes, Collinsella, and Ruminococcaceae. This result suggests that the onset of IBD might be more strongly influenced by environmental factors than by genetic factors, especially with regard to the gut microbiota, which were reduced in IBD patients compared to healthy subjects.

These results suggested that the onset of IBD might be more strongly influenced by environmental factors, especially gut microbiota, than by genetic factors. Moreover, a multi-omics analysis including metagenomic, metatranscriptomic, metabolomic, and other analyses revealed that the gut microbiota and their metabolites in CD and UC were different during the active and remission phases [44].
Click to expand...
Do you the Leona M. and Harry B. Helmsley Charitable Trust? It is a global philanthropy committed to helping people live better lives, inclued curing Crohn’s Disease.They have a lot of projects about Crohn’s Disease.This is a pilot trial of standardized microbiota transplant therapy in Crohn's Disease. It is different from Fecal microbiota transplantation(FMT) that is frequently used in clinical. Maybe the standardized microbiota transplant will be a better treatment,even a way to cure.

https://helmsleytrust.org/grants/regents-of-the-university-of-minnesota-20195778/
 
longzhiwu said:
Do you the Leona M. and Harry B. Helmsley Charitable Trust? It is a global philanthropy committed to helping people live better lives, inclued curing Crohn’s Disease.They have a lot of projects about Crohn’s Disease.This is a pilot trial of standardized microbiota transplant therapy in Crohn's Disease. It is different from Fecal microbiota transplantation(FMT) that is frequently used in clinical. Maybe the standardized microbiota transplant will be a better treatment,even a way to cure.

https://helmsleytrust.org/grants/regents-of-the-university-of-minnesota-20195778/
Click to expand...
thanks for the link! there is a lot of activity in microbiome research for all kinds of diseases. diseases that have been shown to be caused by gut issues. they are on the right path (finally). the future is bright!
 
dysbiosis, a universal cause, a few links of many that i've saved

https://pubmed.ncbi.nlm.nih.gov/34229263/
Supplementation with Bifidobacterium breve BR03 and B632 strains improved insulin sensitivity in children and adolescents with obesity in a cross-over, randomized double-blind placebo-controlled trial All subjects improved metabolic parameters, and decreased weight and Escherichia coli counts. Probiotics improved insulin sensitivity at fasting...

---------------------------------------------------------------------------------------
medical has claimed for years and years that t1 is purely genetic. that meme is fading fast. here they show dysbiosis/leaky gut driving symptoms

and our old friend bifids get a mention. critical family of bugs for all things health

https://pubmed.ncbi.nlm.nih.gov/37062177/
Alterations of the intestinal mucus layer correlate with dysbiosis and immune dysregulation in human Type 1 Diabetes

Findings: Our data show a GB damage with mucus layer alterations and reduced mRNA expression of several mucins (MUC2, MUC12, MUC13, MUC15, MUC20, MUC21) and AMPs (HD4 and HD5) in T1D patients. Mucus layer alterations correlated with reduced relative abundance of short chain fatty acids (SCFA)-producing bacteria such as Bifidobacterium dentium, Clostridium butyricum and Roseburia intestinalis that regulate mucin expression and intestinal immune homeostasis. In T1D patients we also found intestinal immune dysregulation with higher percentages of effector T cells such as T helper (Th) 1, Th17 and TNF-α+ T cells.

=======================================================

hoshimoto (thyroid) disease

https://link.springer.com/article/10.1007/s10238-024-01304-4
====================================================

prostate cancer

https://pubmed.ncbi.nlm.nih.gov/38256945/
======================================================

autism

https://pubmed.ncbi.nlm.nih.gov/38191575/

A robust microbiome signature for autism spectrum disorder across different studies using machine learning Our results indicate that the gut microbiome has a strong association with ASD and should not be disregarded as a potential target for therapeutic interventions.

=======================================================
 
Last edited:
pancreatitis

https://pubmed.ncbi.nlm.nih.gov/38256232/
With the explosion research on the gut microbiome in the recent years, much insight has been accumulated in comprehending the crosstalk between the gut microbiota community and host health. Acute pancreatitis (AP) is one of the gastrointestinal diseases associated with significant morbidity and subsequent mortality. Studies have elucidated that gut microbiota are engaged in the pathological process of AP.
 
depression

https://pubmed.ncbi.nlm.nih.gov/34068832/
Effect of Lacticaseibacillus paracasei Strain Shirota on Improvement in Depressive Symptoms, and Its Association with Abundance of Actinobacteria in Gut Microbiota


We previously reported lower counts of lactobacilli and Bifidobacterium in the gut microbiota of patients with major depressive disorder (MDD), compared with healthy controls.

Depression severity, evaluated by the Hamilton Depression Rating Scale, was significantly alleviated after LcS treatment. The intervention-associated reduction of depressive symptoms was associated with the gut microbiota, and more pronounced when Bifidobacterium and the Atopobium clusters of the Actinobacteria phylum were maintained at higher counts. No significant changes were observed in the intestinal permeability or inflammation markers.

Although it was difficult to estimate the extent of the effect of LcS treatment alone, the results indicated that it was beneficial to alleviate depressive symptoms, partly through its association with abundance of Actinobacteria in the gut microbiota.

============================================

study says this bug makes it through the stomach acid. it's the bug in yakult drink

https://pubmed.ncbi.nlm.nih.gov/10375134/
 
2014 article. again, why is this being ignored by medical?

https://www.hindawi.com/journals/ad/2014/152428/
Autoimmunity and the Gut


10. Conclusion
Factors such as genetics, the environment, infections, and the gut microbiota all play a role in the mediation of autoimmune disorders. There have been tremendous recent advances in our understanding of the interplay of these factors. It is clear that the gut microbiota has a profound and long-term effect starting at birth on the host immune system. It is also evident that it plays a significant role in autoimmune diseases both inside and outside the gut.

There are still questions that remain to be answered: does the immune system shape the gut microbiota or vice-versa? This complex and dynamic symbiosis needs further elucidation and may help in determining the outcome of autoimmune diseases in patients. The clinician can assist the patient by being aware of the triggers of autoimmune disorders and monitoring immune and autoimmune markers in the peripheral blood, thereby being able to take preventive measures to hopefully avert the progression towards an autoimmune disease.
 
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5622781/
Effects of Probiotics, Prebiotics, and Synbiotics on Human Health


Results of clinical studies confirm the positive effect of probiotics on gastrointestinal diseases (e.g., irritable bowel syndrome, gastrointestinal disorders, elimination of Helicobacter, inflammatory bowel disease, diarrhoeas) and allergic diseases (e.g., atopic dermatitis). Many clinical studies have proven the effectiveness of probiotics for treatment of diseases such as obesity, insulin resistance syndrome, type 2 diabetes, and non-alcoholic fatty liver disease.

Furthermore, the positive effects of probiotics on human health have been demonstrated by increasing the body’s immunity (immunomodulation). Scientific reports also show the benefits of the prophylactic use of probiotics in different types of cancer and side effects associated with cancer. Many clinical studies have proven the effectiveness of probiotics, and recommended doses of probiotics are those that have been used in a particular case. Keep in mind that how probiotics work may depend on the strain, dose, and components used to produce a given probiotic product.
 
Last edited:
graphic shows the common cause of several diseases. there are many MANY more that the graphic doesnt include

41423_2018_158_Fig1_HTML.jpg


https://www.nature.com/articles/cmi20187
 
Last edited:
type 2 diabetes

https://pubmed.ncbi.nlm.nih.gov/31936158/
While obesity was once thought to stem from a sedentary lifestyle and diets high in fat, recent evidence supports the idea that there is more complexity pertinent to the issue. The human gut microbiome has recently been the focus in terms of influencing disease onset.

Evidence has shown that the microbiome may be more closely related to T2DM than what was originally thought. High fat diets typically result in poor microbiome heath, which then shifts the gut into a state of dysbiosis. Dysbiosis can then lead to metabolic deregulation, including increased insulin resistance and inflammation, two key factors in the development of T2DM.
 
t2 diabetes again

https://pubmed.ncbi.nlm.nih.gov/31299021/

Recent findings: Recent studies focus on the physiology and molecular pathways of the gut microbiome-host interaction. Short-chain fatty acids (SCFAs) derived from the fermentation of plant-based nonsoluble fiber bind to G-protein-coupled receptors (GPR) GPR 41 and GPR 43 to induce enteroendocrine molecules that control appetite, and to upregulate intestinal gluconeogenesis gene expression that controls glucose regulation. "Metabolic endotexemia" reflects a state of low-grade systemic inflammation that results from lipopolysaccharide (LPS) release from the gut into the systemic circulation in response to a high-fat diet. Inflammatory pathways induced by LPS, activation of toll-like receptor-4 (TLR-4), and other inflammatory signaling pathways are mediators of systemic inflammation, insulin resistance and type II diabetes mellitus.

Summary: Recent scientific data support that derangements in the composition of the microbiota, termed "microbiome dysbiosis" is a factor in the development of "metabolic endotoxemia" and T2DM. Therapeutic options that target the gut microbiome in the treatment of T2DM are explored.
 
a couple of md's wrote books on making their own autoimmunes disappear with gut health

terry wahls wrote 'the wahls protocol' based on what it used to beat multiple sclerosis. i have not read it (yet)

amy myers has books out there describing how she beat her autoimmune. i read one of them - it was similar to what i had done
 
colon cancer. group with more bifids did not have genetic mutation. bifids make butyrate.

https://www.news-medical.net/news/2...-mutations-in-colorectal-cancer-patients.aspx
For about 40% of people diagnosed with colorectal cancer (CRC), the tumor carries a mutation in a gene called KRAS. Many of those mutations have been linked to shorter survival and more aggressive forms of disease. The onset and growth of CRC tumors has also been associated with imbalances in the gut microbiome, but the interplay between these 2 characteristics-;gut dysbiosis and KRAS mutations-;remains poorly understood.

Sequencing revealed 26 different types of gut microbiota that were present in one group but not the other. The genera Fusobacterium, Clostridium and Shewanella were all abundant in the mutant group. Fusobacterium is a Gram-negative microbe found in the GI tract and the oral cavity, and previous studies have connected it to the development of CRC. All 3 of these, the researchers noted, should be considered as non-invasive biomarkers to determine a patient's KRAS status.

Bifidobacterium and Akkermansia were abundant in the samples from patients without a KRAS mutation. Bifidobacterium is a probiotic, and Akkermansia has shown some probiotic activities in previous studies, including suppression of pro-inflammatory factors in the colon. Based on this finding, the researchers speculate that the presence of these bacteria may reduce a person's chance of developing a KRAS mutation and, to an extent, slow the progression of CRC.
 
parkinsons

https://parkinsonsnewstoday.com/news/intestinal-inflammation-markers-linked-parkinsons-risk-study/
Calprotectin, zonulin levels higher in Parkinson’s patients

The gut microbiome is the vast community of friendly bacteria, fungi, and viruses that colonize the gastrointestinal tract and help in its function. Its imbalance, known as gut dysbiosis, can damage the intestinal wall, leading to inflammation.

Previous studies have shown that markers of intestinal inflammation can be detected in blood and stool samples. Parkinson’s disease patients have been found to carry elevated levels of calprotectin and zonulin, a marker of intestinal permeability, when compared with healthy people.
 
prediabetes. low bifids, low butyrate. should we change the title of this thread to 'butyate, the universal protection from disease, eat your bifids, kids'?

https://www.news-medical.net/news/2...iome-differences-in-prediabetic-patients.aspx
The gut microbiome plays a vital role in regulating lipid and glucose metabolism, as gut microbial dysbiosis leads to the development of many diseases. For example, intestinal bacterial composition and abundance changes influence intestinal permeability, which induces insulin resistance and the introduction of bacterial lipopolysaccharides into the bloodstream.

Gut microbial dysbiosis is directly associated with increased gut permeability, which promotes low-grade systemic inflammation. This condition is a key contributor to metabolic syndrome and various chronic diseases, such as type 2 diabetes.

Study findings

The composition, diversity, and abundance of the gut microbiota were significantly reduced in prediabetic patients compared to healthy individuals. This finding was in line with previous studies that indicated differential microbial composition in patients with diabetes.

Consistent with previous studies on type 2 diabetes, the current study reported higher levels of Mediterraneibacter, Bifidobacterium, Blautia, Anaerostipes, Clostridium, and Butyricicoccus in the fecal samples of healthy individuals than prediabetic patients.

Previous studies have shown that butyrate maintains the integrity of the intestinal mucosa. This metabolite is synthesized by gut bacteria, namely, Anaerostipes and Faecalibacterium.

Maintaining the integrity of intestinal mucosa can prevent the invasion of pathogenic bacteria in the blood and the destruction of pancreatic β-cells. This finding indicates the indirect role of Anaerostipes and Faecalibacterium in regulating blood glucose levels.

In contrast to prediabetic samples, healthy fecal samples exhibited high levels of Eggerthella and Streptococcus. However, a higher abundance of Phascolarctobacterium, Bacteroides, Paraprevotella, and Parabacteroides was observed in prediabetic fecal samples.

Prediabetic patients exhibited multiple altered physiological metabolic pathways, which affect insulin transmembrane signaling and overexpression of retinoic acid-inducible gene I (RIG-I). This metabolic dysfunction triggers immune cells to attack β cells, affecting blood glucose levels. Previous studies have also indicated that abnormal sphingolipid metabolism leads to insulin resistance and neuronal apoptosis.

Diet plays a vital role in maintaining gut bacterial diversity and abundance. Therefore, prediabetic patients are advised to consume a low carbohydrate (LC) diet with a higher dietary fiber intake. This combination could improve intestinal barrier integrity, thereby preventing the progression of prediabetes to diabetes
 
this paper gets down to the nuts and bolts. just pasted the conclusion, long paper

https://www.frontiersin.org/journals/immunology/articles/10.3389/fimmu.2022.974305/full
Regulation of gut microbiota-bile acids axis by probiotics in inflammatory bowel disease

4 Conclusions
A large number of studies have revealed the interaction between gut microbiota and BAs. Among them, the intestinal microbiota is involved in BAs synthesis and metabolism, thus influencing BAs composition. Both of which can facilitate the initiation and development of IBD and CAC. Additionally, growing evidence has indicated that certain probiotics exhibit beneficial effects on UC, CAC, and other diseases through multiple mechanisms. In the present review, the possible functional roles of probiotics on gut microbiota-BAs axis were discussed. We laid emphasis on elucidating the alterations of gut bacteria that may involve in gut microbiota-BAs axis in IBD/CAC patients or animal models treated with probiotics.

These elevated bacteria at the genus/species level may include Lactobacillus, Bifidobacterium, Bacteroides, Parabacteroides, Clostridium, Blautia, Bacillus coagulans, Eubacterium, and Eubacterium_fissicatena_group. Some mentioned bacteria that may carry some functional genes seem to have the potential to become probiotic for the moment, but whether they can be used as probiotics still needs numerous and rigorous animal researches and clinical trials according to the four criteria for using as probiotics. Moreover, the activation of BARs, including FXR, TGR5, VDR in monocytes/macrophages cells, DCs, NKT cells, ILC, Th17, and Treg cells, exerts anti-inflammatory and immunomodulatory effects, which may partially explain the positive effects of probiotics on IBD.

According to American Gastroenterological Association Institute’s advice, probiotics may be considered for the treatment of functional symptoms in IBD. The gut dysbiosis existed in IBD may be improved by using probiotics for a period of time. Due to the biological activity and characteristics of probiotics, there are potential risks in the treatment of IBD patients with probiotics, such as bacteremia, transfer of antibiotic resistance, and adverse reactions. Furthermore, the probiotics used for adjunctive therapy may not be effective in some patients on account of individual difference or strain specificity, so it should be discontinued at this time. Therefore, the duration of probiotics should be determined by different therapeutic goals, effects, and actual conditions. In the future, more clinical and animal studies are necessary to explore the direct changes of BAs and specific mechanisms by administration of probiotics in IBD and CAC
 
strong evidence they say. dont see that very often on pubmed

https://pubmed.ncbi.nlm.nih.gov/38585636/
An advanced search considered clinical studies on probiotic for IBD from inception to 2023 in PubMed, Embase, Cochrane Library, and Web of Science.

In the treatment of UC with probiotics, only Escherichia coli Nissle 1917 for maintenance treatment of UC in remission, and Bifidobacterium and VSL#3 for induction of remission in patients with mild to moderately active UC have shown strong evidence.
 
possible pathogen

https://pubmed.ncbi.nlm.nih.gov/36968108/
Currently, gastrointestinal infection has been proposed as one initiating factor of CD. Yersinia enterocolitica, a zoonotic pathogen that exists widely in nature, is one of the most common bacteria causing acute infectious gastroenteritis, which displays clinical manifestations similar to CD. However, the specific role of Y. enterocolitica in CD is controversial.
 
study published this week. they find dysbiosis in crohns - and that dysbiosis correlated with 'lifestyle'

https://pubmed.ncbi.nlm.nih.gov/38656971/
Gut microbiota composition in patients with Crohn's disease in Saudi Arabia

The results were correlated with the demographic and lifestyle information, which the participants provided via a questionnaire. α-diversity measures indicated lower bacterial diversity and richness in the active and inactive CD groups compared to the control group.

Greater dysbiosis was observed in the active CD patients compared to the inactive form of the disease, showed by a reduction in microbial diversity. Specific pathogenic bacteria such as Filifactor, Peptoniphilus, and Sellimonas were identified as characteristic of CD groups. In contrast, anti-inflammatory bacteria like Defluviitalea, Papillibacter, and Petroclostridium were associated with the control group.
 
another one from this week. interesting that they created four distinct groups of ibd people based on their microbiomes alone. that could give us some clues

https://www.tandfonline.com/doi/full/10.1080/07853890.2024.2338244?src=exp-la
Fecal microbiota is associated with extraintestinal manifestations in inflammatory bowel disease

Gut microbiome perturbation is a well-established characteristic of IBD, characterized by lower diversity (compared with healthy subjects) and a depletion of short-chain fatty acid-producing obligate anaerobes, such as Roseburia spp. and Faecalibacterium prausnitzii and an increase in Escherichia coli and Ruminococcus gnavus [Citation12,Citation13].

Mar et al. found that UC patients could be stratified into four distinct groups based on the composition of their gut microbiota [Citation14]. Notably, these groups exhibited significant differences in both disease severity and the presence of EIMs [Citation14], providing initial evidence of a relationship between the gut microbiome composition and EIMs.
 
leaky gut precedes crohns. this is big and needs to be well known so that people can take measures to reverse/prevent

https://crohnsandcolitis.ca/News-Events/News-Releases/GEM-Study-Links-Leaky-Gut-to-Crohn-s-disease
GEM Study Links Leaky Gut to Crohn’s Disease

International project led by Crohn’s and Colitis Canada is getting us closer to preventing Crohn’s disease and ultimately, a cure

TORONTO, ON – August 20, 2020 – Crohn’s and Colitis Canada is pleased to announce that the world-renowned Genetic, Environmental, Microbial (GEM) Project has led to a significant finding.

The study found that healthy first-degree relatives of Crohn’s disease patients, who eventually developed Crohn’s disease themselves, had abnormal LacMan ratios when enrolled in the study. Gut barrier integrity was measured using Lactulose Mannitol Ratio or LacMan ratio. Lactulose is a large sugar that normally does not cross the gut barrier. Higher levels of lactulose in the urine is suggestive of a leaky gut.

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.
 
Last edited:

Similar threads

C
children, crohns, and gut health
Replies
2
Views
1K
cheka
C
Crohn2357
GUT STERILIZATION FOR CROHN’S DISEASE (THEORETICAL CURE)
Replies
2
Views
1K
cheka
C
A
GlycanTrigger's 6-year project
Replies
4
Views
2K
Andersen007
A
kiny
Unfermented β-fructan Fibers Fuel Inflammation in Select Inflammatory Bowel Disease Patients
Replies
38
Views
4K
kiny
kiny
kiny
Crohn's disease happens in clusters, and no one knows why.
Replies
4
Views
1K
asadmom
A

Latest posts

Back
Top