Swapping Poo Fixes IBD (in children so far)
In numerous earlier posts I have explored the emerging evidence as well as the historical experiences for the use of faecal microbial transplantation (FMT) and the management of complex dysbiotic gastrointestinal tracts: this is also sometimes called faecal transplant therapy (FTT)
Whilst the greatest amount of data on this therapy is available with reference to the successful (>92%) treatment of clostridium difficile infection, others have been exploring its potential treatment in regard to other complaints related to dysbiosis of the gastrointestinal flora.
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Autoimmunity and the Worm
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An immunologist, Dr Joel Weinstock provoked mixed reactions from the scientific community when he suggested that in line with Strachan’s hygiene theory[1] and Rook’s ‘old friend’s theory,[2] that the removal from the western world of helminths, had provided the opportunity for inflammatory diseases of the bowel and elsewhere to increase in frequency.[3] 20 years on from Strachan’s first proposals and Weinstock’s hypothesis have been examined in human trials and found to be effective, and the human microbiome project has uncovered other interesting relationship’s.[4]
Faecal Transplant (FT) and IBD
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I have explored the role of appropriate transplantation in the resolution of MRSA infection that fails to resolve with antibiotic therapy, and have intimated that other conditions of the bowel and linked tissues may also benefit. The model is: that loss of mucosal tolerance underlies the pathology of inflammatory bowel disease and is also linked to irritable bowel syndrome. These altered states of function reflect a combination of environmental, genetic and emotional events that coalesce into a wide range of conditions.
Milk Fats Plus Bacteria = Gut Inflammation
It is a global phenomenon – the increase in gastrointestinal inflammatory disease over the last 50 years, so fast is this occurring that genetic drift is very unlikely to be attributable as causal; but it is likely that changes in diet and lifestyle amongst the genetically susceptible act as triggering agents to induce aberrant immune responses that lead to inflammatory bowel disease and other systemic inflammatory illnesses.
In a fascinating study published in Nature on the 13th June in their letters section a group of researchers show how the inclusion of fats derived from ilk, change the bacterial composition in the gastrointestinal tracts of mice promoting the development of colitis.[1]
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Apples Can Suppress IBD
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Here’s another reason why “an apple a day keeps the doctor away”—according to new research findings published in the Journal of Leukocyte Biology (https://www.jleukbio.org), oral ingestion of apple polyphenols (antioxidants found in apple peels) can suppress T cell activation to prevent colitis in mice.[1] This study is the first to show a role for T cells in polyphenol-mediated protection against an autoimmune disease and could lead to new therapies and treatments for people with disorders related to bowel inflammation, such as ulcerative colitis, Crohn’s disease and colitis-associated colorectal cancer.
Antibiotics and IBD in Childhood
Inflammatory Bowel Disease such as Ulcerative Colitis and Crohn’s blight people’s lives and restrict their functionality. The formative years of our lives represents the time when microbiological partnerships are being formed to provide lifelong co-dependence on each other. The role of the microbiota in immune tolerance in the gut and elsewhere is increasingly understood but is still an area rich for investigation.
In this study of Danish children a nationwide cohort study was conducted of all Danish singleton children born from 1995 to 2003 (N=577,627) with individual-level information on filled antibiotic prescriptions, IBD and potential confounding variables.[1] Using Poisson regression, rate ratios (RRs) of IBD were calculated according to antibiotic use. Antibiotic use was classified according to time since use, type, number of courses used and age at use.
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Is that Iron Supplement Making Your IBD Patient Ill?
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Iron replacement therapy is a common treatment in patients with anaemia and Crohn’s disease, but oral iron supplements are less tolerated. The pathogenesis of Crohn’s disease is attributed to intestinal bacteria and environmental factors that trigger disease in a genetically predisposed host. The aim of this study was to characterise the interrelationship between luminal iron sulfate, systemic iron, the gut microbiota and the development of chronic ileitis in a murine model of Crohn’s disease.[1]
Broccoli Intake Influences IBD Pathology in Crohns Disease.
A dietary selection of more traditional fibre rich foods especially broccoli, appears to confer an immunological advantage to those patients suffering from the inflammatory bowel disease: Crohn’s. A paper published in the prestigious journal GUT recognised that Crohn’s is more common in industrialised nations than in those eating a more traditional diet. The study demonstrates that modern food ingredient called polysorbate 80 increases inflammation by altering the barrier integrity.[1]
Polysorbate 80 is a nonionic surfactant and emulsifier derived from polyethoxylated sorbitan and oleic acid, and is often used in foods. Polysorbate 80 is a viscous, water-soluble yellow liquid.
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Genes, Viruses, Microbes and IBD
Crohn’s disease is common and miserable to suffer from, yet its actual cause is still under some debate as no clear understanding has yet been fully elucidated. It is known that there are some gene variations and that the environment has an impact. A paper out in Cell suggests, based on a mouse model that it may be a virus that makes the difference between health and inflammation. demonstrate that a viral infection, a toxic insult to the gut, commensal bacteria, and a Crohn’s disease susceptibility gene collude to cause inflammatory disease in the mouse gut.[1]
To be clear, Cadwell and co-workers are not arguing that Crohn’s disease is caused by infection with norovirus (as used in this study) or by any other single microbe. The environmental factors that predispose to and protect from Crohn’s disease remain uncertain, but the balance among commensal and pathogenic gut bacteria and viral infections is likely to be part of the story. These studies make an urgent and compelling case for characterising the human virome as well as the microbiome and defining its effects on physiology and gene expression. In addition, further explanations to help us to understand how the virome interacts with polymorphisms in the host genome and how numerous toxins in the environment alter this complex interplay will need to be unravelled.
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IBD and Environmental Triggers- Vegetable Gardens Vs Genes
Crohn’s and Ulcerative colitis are understood to have a number of genetic related risks, but increasingly scientists are having to accept that our double helix does not predict our health risks except in a few single gene diseases such as cystic fibrosis, the haemoglobinopathies. In fact the enormous endeavours and resources spent pursuing this elucidation have produced surprisingly modest practical benefits.
Even when dozens of genes have been linked to a trait, both the individual and cumulative effects are surprisingly small and nowhere near enough to explain earlier estimates of heritability.[1]
The recent discovery by a New Zealand group that there are a number of childhood factors associated with the development of Inflammatory Bowel Disease, further supports the concept that environment – in this case during childhood plays an important role in modulating the risk for developing these conditions. The rising incidence of these diseases over the last 50 years also supports the role of environment, as genes take many hundreds of years to change.[2]
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