Antibiotics and IBD in Childhood

Wednesday, 09 March 2011 by
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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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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]

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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

Monday, 09 August 2010 by
Reading Time: 3 minutes

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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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]

Vitamin D Vs Crohn’s (IBD) & Cancer

Wednesday, 10 February 2010 by
Reading Time: 2 minutes

Crohns disease is an inflammatory disease of the intestines that may affect any part of the gastrointestinal tract from anus to mouth, causing a wide variety of symptoms. It primarily causes abdominal pain, diarrhoea (which may be bloody), vomiting, or weight loss, but may also cause complications outside of the gastrointestinal tract such as skin rashes, arthritis and inflammation of the eye.[1]

A new study has found that Vitamin D, readily available in supplements or cod liver oil, can counter the effects of Crohn’s disease.[2]

The data collated in this study suggests, for the first time, that Vitamin D deficiency can contribute to Crohn’s disease. Epidemiologically it had already been noted that people from northern countries, which receive less sunlight, necessary for the fabrication of Vitamin D by the human body, are particularly vulnerable to Crohn’s disease.[3]

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Phosphatidylcholine (PC) is a major lipid of the gastrointestinal mucus  layer. We  recently showed  that mucus from patients suffering  from ulcerative colitis  has low levels of PC. Clinical studies reveal that the therapeutic addition of PC to the  colonic mucus using slow release preparations is beneficial.

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Comment: The enzyme, coded for by the MEP1A gene, is a zinc-containing metalloprotease called meprin, and is abundant in the intestine. A protease is an enzyme that breaks down proteins in the body. he researchers concluded that a particular defect in the MEP1A gene is an indicator of vulnerability to IBD, particularly ulcerative colitis. The