IBS And Food – Is There A Link?
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There is a growing body of evidence to suggest that certain dietary constituents exacerbate symptoms and perhaps contribute to the pathogenesis of IBS. Patients have long associated their IBS symptoms with the ingestion of certain foods, combinations of foods, or generally with meals. Response rates from elimination diets have ranged from 15%-71%,[1] with wheat, milk, and eggs being the most commonly implicated foods.
IBS Succesfully Managed by Nutritional Therapy
It will be of no real surprise to know that the incidence of irritable bowel syndrome (IBS) is common. Around the world it is estimated that some 10-20% of the population suffer from it. This is not an inconsequential number, and apart from the miserable statistics, it comes with loss of function, misery, anxiety, pain, bloating, altered bowel habits and loss of quality of life.
Whilst a clear explanation of the cause remains somewhat elusive, there is an increasing acceptance that the relationship between the brain-gut axis, central nervous system, peripheral stress response, infection, dysbiosis, barrier defects, inflammation and immune imbalance play significant roles in the causation.
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Is this a Perfect Functional Meal for Mucosal Tolerance?
Stewed apples as medicine
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Dientamoeba Fragilis is it Really a Problem
Dientamoeba Fragilis
First, some background to this parasite and a brief discussion of what may be used pharmaceutically and then a review of how a non-drug approach may be applied through the understanding of the mechanisms employed by the organism and its relative susceptibility to eradication strategies.
Dientamoeba fragilis (D. fragilis)is a trichomonad (a genus of anaerobic protists that are parasites of vertebrates) parasite found in the gastrointestinal tract of humans and implicated as a cause of gastrointestinal disease. D. fragilis has been found in most parts of the world in both rural and cosmopolitan areas. Infection with D. fragilis is called Dientamoebiasis and is associated variously with symptoms of abdominal pain, diarrhoea, weight loss, and fever.[1]
Dientamoeba fragilis is a parasite that causes gastrointestinal problems. Despite its name, Dientamoeba fragilis is not an amoeba but a flagellate. This protozoan parasite produces trophozoites; cysts have not been identified. Infection may be either symptomatic or asymptomatic.
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Specialised Protein Operates Independantly of Bacteria to Induce Mucosal Tolerance
The unfolding of bacterial homeostasis in the gut continues apace and with each new stone uncovered there are interesting pathways that provide avenues for exploration and explanation in the management of inflammatory bowel diseases and functional disorders.
A paper out in Science[1] has identified that the protein β-catenin has an important role to play in inflammation control (β-catenin is part of a complex of proteins that constitute adherens junctions (AJs). AJs are necessary for the creation and maintenance of epithelial cell layers by regulating cell growth and adhesion between cells) plays an important role in the management of mucosal tolerance.
β-catenin signalling promotes the induction of regulatory T (TReg) cells while suppressing T helper 1 (TH1) and TH17 cells in the gut by maintaining intestinal dendritic cells (DCs) in a tolerogenic state.
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Mechanism of Fatty Acids Anti Inflammatory Effects – Explained?
Most Nutritional Therapists are comfortable in the concept and application of concentrated essential fatty acids especially fish oils as a means of altering abnormal inflammatory pathways in the body. Some EFA’s are perceived to be anti-inflammatory and others pro-inflammatory. Whilst the simplistic dichotomy of interpretation (Omega 3 Anti/Omega 6 Pro) has kept many a student content that they have mastered the art of complex fatty acid biochemistry – the reality is that cell membranes operate in a state of competitive inhibition with fatty acids of all carbon chain lengths and their role is highly sophisticated and complementary.
So…the paper out in the journal Cell this month (Sept 2010) from the lab of Prof. Olefsky at the University of California is a really exciting addition to the extensive research available – in that it elegantly describes a key anti-inflammatory mechanism using a G-protein coupled receptor.[1]
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Massage Beneficially Impacts Immune Response.
There are very few people that do not like to have a massage, and those of us that do – me, me, me, now have an extra justification for throwing yourself onto the nearest couch and shouting “fetch the oil, I’m ready for basting”.
Published in the Sept Journal of Complementary and Alternative Medicine 2010 a paper suggests that a single session of Swedish Massage Therapy produces measurable biologic effects.[1] The intervention tested was 45 minutes of Swedish Massage Therapy versus a light touch control condition, using highly specified and identical protocols.
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Is There A Rural/Urban Gradient In The Prevalence Of Eczema? A Systematic Review And What Can Be Done About It?
One in 10 schoolchildren in the western world suffers from eczema and even developing nations have also seen an increasing trend in the last few decades. There are many proposals to explain the increased incidence, one area of relevance is the environmental impact. Falling under the often misused ‘hygeine hypothesis’ title it has been proposed that there is a reflective difference in the gradient between rural and urban children. Implying the environmental impact on the developing immune system of children is different and therefore less protective in the urban setting.
This concept has now been studied in a recent article in the British Journal of Dermatology.[1] By conducting a Medline and Embase data base review studies that compared the incidence between the two environments were reviewed. Some 26 papers were assessed with 19 demonstrating a higher risk for eczema in an urbanised area, of these 11 were regarded as being statistically significant. A further 6 studies showed a lower risk of eczema in an urbanised area, of which just 1 was statistically significant.
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Neurological/Dietary Control Over the Immune System – The Role of Fats
The immune system in humans and animal is complex, all the more so because it crosses over all tissues. The traditional view has been that the immune system keeps itself in check, and that is mostly the case. However, for some years there has been a development of a neural feedback loop comprehension that helps to answer some of the complex mechanisms and remarkably ties in the role of a nutritional strategy for immune management. This is known as the inflammatory reflex.
The inflammatory reflex, a prototypical neural circuit that modulates innate immunity, is activated by the presence of cytokines or other inflammatory products in tissues that triggers afferent (a nerve that passes impulses from receptors toward or to the central nervous system) action potentials travelling in the vagus nerve. The ascending information is relayed to brainstem nuclei that control efferent (nerves that convey nervous stimulus from the brain to other parts) neural signals in the form of action potentials transmitted back to the periphery via the vagus nerve.
Whilst this may sound complex – few subjects that combine neurology and immunology aren’t… the outcome suggested meets simple strategies, based on complex mechanisms.
A Bacteria Triggers Arthritis.
The gut microbiomes of humans and mice are broadly similar which is helpful as this paper has used the mouse model to explain how a resident bacteria in the gut can induce arthritis. In both hosts human and mouse upwards of ∼1000 different microbial species from ∼10 different divisions colonise the gastrointestinal tract, but just two bacterial divisions—the Bacteroidetes and Firmicutes—and one member of the Archaea appear to dominate, together accounting for ∼98% of the 16S rRNA sequences obtained from this site.[1] 16SrRNA is a laboratory method for analysing bacterial and provides species-specific signature sequences useful for bacterial identification but is not routinely used in diagnostic settings yet.
Their analysis revealed that despite the enormous species variation in the gut a single species of bacteria that lives here is able to trigger a cascade of immune responses that can ultimately result in the development of arthritis.[2] Gut-residing bacteria can also play a role in disorders of the immune system, especially autoimmune disorders in which the body attacks its own cells. The gut microbiota is now known to shape intestinal immune responses during health and disease with systemic effects.
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The immune system is prone to the same grave misfortunes as any defense system handling weapons: collateral damage that comes with the destruction of the enemy on one’s own territory and friendly fire due to mistaken identity. Whereas the collateral damage is the price we pay for clearance of infections, autoimmunity is a pathological process. Nevertheless, the effector mechanisms involved in both processes are the same. Whether environment can be a cause, a trigger or an amplifier of an autoimmune disease are questions that are being intensively investigated.
