May 2016 saw the publication of an open access article, that beautifully captures the zeitgeist of how the food we eat, the microbiome we possess, the genes we express and the metabolomics information we produce coalesce into a risk benefit model.[1]
The abstract states:
It is now convincingly clear that diet is one of the most influential lifestyle factors contributing to the rise of inflammatory diseases and autoimmunity in both developed and developing countries. In addition, the modern ‘Western diet’ has changed in recent years with increased caloric intake, and changes in the relative amounts of dietary components, including lower fibre and higher levels of fat and poor quality of carbohydrates. Diet shapes large-bowel microbial ecology, and this may be highly relevant to human diseases, as changes in the gut microbiota composition are associated with many inflammatory diseases. Recent studies have demonstrated a remarkable role for diet, the gut microbiota and their metabolites—the short-chain fatty acids (SCFAs)—in the pathogenesis of several inflammatory diseases, such as asthma, arthritis, inflammatory bowel disease, colon cancer and wound-healing. This review summarizes how diet, microbiota and gut microbial metabolites (particularly SCFAs) can modulate the progression of inflammatory diseases and autoimmunity, and reveal the molecular mechanisms (metabolite-sensing G protein-coupled receptor (GPCRs) and inhibition of histone deacetylases (HDACs)). Therefore, considerable benefit could be achieved simply through the use of diet, probiotics and metabolites for the prevention and treatment of inflammatory diseases and autoimmunity.
Comment
Many papers are published on the microbiome and food these days, but these authors have presented a very comprehensive narrative review to help connect many aspects of human health and function by using a systems approach.
Reference
[1] Richards JL, Yap YA, McLeod KH, Mackay CR, Mariñ E. Dietary metabolites and the gut microbiota: an alternative approach to control inflammatory and autoimmune diseases. Clinical & Translational Immunology (2016) 5, e82 View Full Paper
