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BJNThe British Journal of Nutrition published a review paper in July 2015, exploring the relationship between inflammation, diet and health. Whilst this is neither new nor novel, the momentum is becoming clear. There is a steady awareness in research that the consumption of certain foods and the absence of others contributes to a provocative change in defence molecules with the result that many of the non-communicable diseases that blight western health care can develop and thrive.

This open access article is well worth saving for those refresh reads.[1]

The importance of chronic low-grade inflammation in the pathology of numerous age-related chronic conditions is now clear. An unresolved inflammatory response is likely to be involved from the early stages of disease development.

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indexThe growing knowledge in research communities concerning the symbiotic relationship we have with our bacterial organism population is increasingly reflecting that which we have been discussing for many years – namely the use of antibiotics (and many of our current lifestyle habits) is not a benign event in terms of microbiome outcomes. It seems that even short pulses of widely used antibiotics (amoxicillin and tylosin in this paper) can lead to long-term development changes in mouse pups, including increased body mass and bone growth and changes to the gut microbiota, according to a study published in Nature Communications.[1]

Oh Boy… the journal Nature has this week (9.10.14) identified the insidious effect of consuming ‘diet’ or non caloric sweeteners on the burgeoning mass of human adipocytes and they have really taken a good run at it.[1]

Non-caloric artificial sweeteners (NAS) were introduced over a century ago as means for providing sweet taste to foods without the associated high energy content of caloric sugars. NAS consumption gained much popularity owing to their reduced costs, low caloric intake and perceived health benefits for weight reduction and normalization of blood sugar levels.[2] For these reasons, NAS are increasingly introduced into commonly consumed foods such as diet sodas, cereals and sugar-free desserts, and are being recommended for weight loss and for individuals suffering from glucose intolerance and type 2 diabetes mellitus.

Psoriasis, Diet and Food Concentrates

Thursday, 25 September 2014 by | Comments: 1

It has been argued in many cases quite vehemently that diet has no role to play in many of the common dermatological conditions that trouble people. Yet as no surprise to those who use changes in diet to assist skin management a number of studies are now confirming that seen in empirical practice – your food choice and supplement choice influences for the better or worse skin health.[1],[2]

The two papers above are useful summaries of interventions that may add improvement to the skin damage or may mitigate associated disease risk or medication side effects. Clearly as food has multiple points of intervention in human physiology, even those conditions with a high genetic association are also going to be advantageously influenced by the correct management of body health via food and food concentrates.

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The condition – Nonalcoholic steatohepatitis (NASH) is increasing in prevalence, in tandem with the obesity epidemic, in both children and adults. Identifying specific dietary components that drive NASH is important for successful management of this disease.

Nonalcoholic fatty liver disease (NAFLD) encompasses a range of liver diseases. Simple steatosis, or fatty liver, is now found in up to 31% of adults[1] and 16% of children.[2] Of those with steatosis, approximately 5% will develop nonalcoholic steatohepatitis (NASH), in which steatosis is accompanied by inflammation and fibrosis.[3] Up to 25% of NASH patients will progress to cirrhosis. NASH is the third leading indication for liver transplantation in the United States and will become the most common if current trends continue.[4] Therefore, understanding its pathogenesis and treatment is of utmost importance.

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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.

The research, published in Lancet Oncology and carried out at the International Agency for Research on Cancer, studied international data for 27 cancers in 184 countries in order to identify the factors which contribute to the development of the diseases. The results suggest that 16% of all cancers are a result of infections, and of that sub-set 80% occur in less developed regions.[1]

The WHO another data crunching megalith estimates that 6% of cancers in wealthy nations and 22% in low- and middle-income countries are caused by infectious agents: viruses such as HBV, HPV and hepatitis C virus (HCV), bacteria such as Helicobacter pylori and waterborne parasites.

At present no chronic disease has a greater drag on global function than mental illness.[1] A remarkable 40% of the European population is affected in any given year with depressive symptoms, and these numbers are rising.

Core symptoms include depressed mood, anhedonia (reduced ability to experience pleasure from natural rewards), irritability, difficulties in concentrating, and abnormalities in appetite and sleep (‘neurovegetative symptoms’). In addition to mortality associated with suicide, depressed patients are more likely to develop coronary artery disease and type 2 diabetes. Depression also complicates the prognosis of a host of other chronic medical conditions. The chronic, festering nature of depression contributes substantially to the global burden of disease and disability.

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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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Microbes Are What You Eat

Thursday, 14 July 2011 by

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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