Microbes and Us
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Over the past several years, studies have revealed an astonishing diversity in our so-called microbiome. A five year project utilising researchers from around the world has been constructed to identify our mutual cohabitants that define our microbiome.[1] In Europe the MetaHIT project has pulled 8 countries and 13 academic partners together to add further data to this project.[2]
Food and Our Bacterial Mix – Can we really change them both?
A few weeks ago (June 2012), a paper in Nature by a group of researchers suggested that despite the vast geographical and nutritional differences in the human population, that just three predominant bacterial clusters (referred to as enterotypes hereafter) could explain all of our gastric microbial mixes.[1] This they suggest indicates the existence of a limited number of well-balanced host–microbial symbiotic states that might respond differently to diet and drug intake.
Each of these three enterotypes are identifiable by the variation in the levels of one of three genera: Bacteroides (enterotype 1), Prevotella (enterotype 2) and Ruminococcus (enterotype 3). These enterotypes are not as sharply delimited as, for example, human blood groups; they are, in contrast, densely populated areas in a multidimensional space of community composition. They are nevertheless likely to characterise individuals, in line with previous reports that gut microbiota are quite stable in individuals and can even be restored after perturbation.[2]
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Bugs, Guts and Research
For the majority of the last 100 years the role of bacteria in human health has been explored in terms of risk to health and well-being, the ‘bad bug = bad health’ paradigm. The result has been a combination of remarkable benefits against infectious related deaths and a slow but steady development of chronic non communicable diseases (CNCDs) – cardiovascular disease, cancer, diabetes and respiratory diseases now kill more people worldwide than all other diseases combined.
This rate of demise will continue to rise in the coming years as the global population ages, sedentary lifestyles and inappropriate food consumption continues to spread across the world.
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Microbes Are What You Eat
Most nutritional therapists and others that regard the role of the bacterial populations in the human gut as being a significant part of our capacity to operate and function in health or otherwise, understand that food choice has an effect.
A recent study on mice published in Science raises some very interesting early observations.[1] The same group published an earlier study exploring the same strategy.[2] Aware that food choices alter bacterial colony ratios and may favour certain bacterial species over others, mice were impregnated with a small number of commonly found human bacteria (10) and then were fed, via human pureed baby food concentrations of 4 commonly consumed ingredients. The researchers state that some 60% of the variation in species is attributable to dietary food choice.
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Probiotics and Lecithin cause heart disease?
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Diet, intestinal bacteria and liver metabolism to the generation of a chemical that promotes the build-up of arterial plaque and cardiovascular disease is the proposal in the alarmingly interesting paper published in the internationally respected Journal; Nature.[1] What we shout, how can two not simply innocuous but beneficial agents gang up to contribute to the cause of the world’s leading promoter of disease and death? Read on to find out..
Gut Flora, Probiotics and Vitamins A+D – Do they influence Allergy and Autoimmunity.
Michael Ash BSc, DO, ND FDipION
The fields of immunology, microbiology, nutrition, epigenetics and metabolism are rapidly converging utilising a systems biology methodology to explain our intimate relationships with our microbial cohabitants. For over 30 years data has been building to scientifically support the hypothesis that intestinal cohabitants operate in a collective manner with macro and micro food intakes to shape and define our immune systems from an early age. The result is a collective impact bound by mutual cooperation that may have unintended consequences including a wide range of pathologies.
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Asthma and Bugs a Marriage Blessed in Muck
Those of us living in the country and in contact with farms and farm animals are being blessed with an immune priming experience for free – other than the cost of washing the clothes!
The exposure to bacteria, fungi and other microbes confers to us a unique advantage in the reduction of asthma and atopy incidence compared to children who never have farmyard contact and has previously been reported as such.[1]
I can see some innovative farmers seeking to promote a day out at their farms as an immune priming experience in the future a sort of ‘Farm Yard Atopy Camp’ for all children under 5 with a guaranteed cowlick experience!
A dirty weekend away will start to lose its cachet amongst the older family members and represent a weekend of juvenile delights in which washing behind the ears will be postponed for a little while.
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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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Dendritic Cells Aid Intestinal Homeostasis and Disease
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Inside our gastrointestinal tract live a family of specialised cells, co-dependent on bacteria and nutrients to send a calming message to the mucosal tissues. They have a number of variations in their make up but they are vital in their role as diplomats, passing sensitive information across the borders to provide a long term peaceful mission and maintain oral tolerance. Essentially they induce either protective immunity to infectious agents or tolerance to innocuous antigens, including food and commensal bacteria. This recent article out in the Journal of Clinical Investigation explores the current understanding of how these cells contribute to health and illness.[1]
Vegas, Pregnancy, Immunity and Allergy Prevention!
The saying is ‘what happens in Vegas stays in Vegas’, or if you are English ‘what happens in Blackpool….’ but the same cannot be said about what happens in utero, as increasing evidence supports the understanding that the maternal nutritional environment and early feeding affects the health of the foetus beyond infancy and into adulthood.[1],[2] An article in Nature’s Mucosal Immunology this month explores some of the key events in foetal and neonatal immune management.[3] It stimulated a revisit to the area of what to consider for parents to be and mums of young children when they ask ‘is there anything I can do to prevent or reduce the risk of allergy or atopy in my child’.
The first moments, weeks and months of life can determine the health outcomes of an individual over the duration of their lifetime and this knowledge represents a significant choice for prospective parents. Fortunately the remarkable adaptability of the immune and central nervous system means that there are numerous opportunities in the early years of life to positively influence health outcomes even if the early stages were less than optimal.
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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.
