Bile acids are critical for the digestion and absorption of fats and fat-soluble vitamins in the small intestine. Recent studies suggest bile acids have further functions as pleotropic signalling metabolites able to interact with germline-encoded host receptors and microbiota to regulate an array of #metabolic and #inflammatory pathways. Researchers from The Scripps Research Institute Florida and Osaka University Japan have recently published a piece discussing the interplay between bile acids, the microbiota and the mucosal immune system. They focus on how this interplay can regulate intestinal homeostasis and inflammation. The dynamic three-dimensional interplay between #bile acids, the microbiome and the mucosal immune system represents an important new frontier in the field of Mucosal Immunology. 

Dr Carrie Decker ND explores the relative risk of generating an adverse response to sugars and the environmentally related triggers.

Associated with the recent World Health Day of 8th April 2016 the first “Global Report on Diabetes” was published by the World Health Organization (WHO). The statistics on diabetes highlighted in this publication are alarming: diabetes has almost quadrupled since 1980 from 108 million to an estimated 422 million adults; diabetes is the number one cause of death, with 1.5 million people directly dying associated with diabetes in 2012.  More than 43% of these deaths occurred in individuals under the age of 70 years old. The increase in type-2 diabetes (T2DM) has been observed to mirror the increasing prevalence in individuals who are overweight and obese. These numbers are also concerningly high, with 1 in 3 adults over the age of 18 being overweight and 1 in 10 being obese.[1]  

Recent studies have suggested that gut bacteria play a fundamental role in diseases such as obesity, diabetes and cardiovascular disease. Data are accumulating in animal models and humans suggesting that obesity and type 2 diabetes (T2D) are associated with a profound dysbiosis.[1]

First human metagenome-wide association studies demonstrated highly significant correlations of specific intestinal bacteria, certain bacterial genes and respective metabolic pathways with T2D. Importantly, especially butyrate-producing bacteria such as Roseburia intestinalis and Faecalibacterium prausnitzii concentrations were lower in T2D subjects.

Unless you have been living in a far flung part of the world where access to data is limited most people are aware that sugar has finally been determined to be a far more problematic part of human health decline and disease risk that the much trumpeted but now derided role of fats. Recently poularised opinions, driven by scientists such as Robert Lustig and communicated via films such as Fed Up have in the minds of many made sugar the new tobacco.

The use of Saccharomyces Boulardii as a therapeutic intervention in people with alterations in their microbiota and local immune responses has been explored for over 50 years. The multiple points of action this simple yeast initiates in terms of mucosal barrier function and immune competence has made it an attractive and safe product for many clinicians. This study published in Jun 2014 in the American Society for Microbiology explores its role in a mouse model, but opens some interesting prospects for human health.[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.

New research in The FASEB Journal suggests that the postprandial levels of circulating metabolites in the blood of identical twins tends to be similar after a fast food meal, independent of weight difference.

If you think losing weight is enough to prevent Type 2 diabetes, don’t get your hopes up. A new research report in September 2014 issue of The FASEB Journal, suggests that you don’t have to be overweight to develop Type 2 diabetes. [1] This study compared genetically identical twins-one heavier and one leaner-and found that after eating a fast-food meal, the circulating metabolites, including those related to Type 2 diabetes, were found in both individuals at the same levels. These findings suggest that the onset of this type of diabetes is largely influenced by genetic factors and/or the composition of gut microbiota.

Eating cheese and other full fat dairy foods appears to confer an advantage in risk for the incidence of type 2 diabetes. Risk of developing this common disease declined significantly as levels of a fatty acid found in whole-fat dairy products increased, data from a recent large cohort study showed.[1]

Those adults that were found to have the highest levels of trans-palmitoleic acid had a remarkable 60% lower diabetes incidence compared with individuals who had the lowest levels. Risks for metabolic syndrome were also reduced in those with the higher TPA levels – as one might expect.

Whilst statistical analysis of demographic, clinical, and lifestyle factors showed that whole-fat dairy consumption had the strongest association with levels of trans-palmitoleate there is still some uncertainty about the correlation.

I think we all accept that changes in insulin levels over time predispose people to the development of type II diabetes and that this is often accompanied by the central adiposity that distinguishes the metabolic syndrome morphology we have come to look for.

This study, published in PLOS One this year (2010), suggests that besides these clinical indications another slightly less obvious change to body mass affects insulin resistance and increases risk of diabetes.[1]

A series of papers out in the New England Journal of medicine on March the 14^th 2010 have failed to add any substantive weight to the use of medication in the prevention of diabetes and cardiovascular disease. [1]^,[2],[3]

The continued expansion of the western global waistline and incidence of diabetes has provided fertile opportunity for a wide range of clinical trials designed to uncover strategies for incidence of diabetes reduction.[4] There is no surprise in the discovery that making significant changes to people’s lifestyles, eating less and being more active, the primary causes of weight gain, also have a consistent reduction in type II diabetes risk. The real success has also been in the associated benefits in reduction of related cardiovascular disease risk[5] and raising of mood.[6]