Rheumatoid arthritis! – these are not the words anyone wants to hear when they start to experience joint discomfort. It quite naturally engenders fear and worry as the tretaments offered are in themselves a challenge in most cases and avoiding effective treatment can predispose an individual to a shortened and miserable life.

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The journal Scientific American in their June 2012 issue looked at the social network of the bacteria in our digestive tract and on our skin. As I have previously stated the role of our commensal bacteria as significant players in our health and function is becoming more and more understood. Whilst those of us involved

Whilst the findings may seem consistent with our current understanding of the relationships between the gastrointestinal tracts bacterial maturation and immune functionality – the relationship between competence and breast milk, from a neonate’s immune perspective has been expanded following the publication of this study in Genome Biology.[1]

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]

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]

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.

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.

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..

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.

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.