Thursday, October 20, 2016

Visceral Fat Not Only An Alien Invader, It's a HERITABLE Alien Invader!!!


biomedcentral |  Variation in the human fecal microbiota has previously been associated with body mass index (BMI). Although obesity is a global health burden, the accumulation of abdominal visceral fat is the specific cardio-metabolic disease risk factor. Here, we explore links between the fecal microbiota and abdominal adiposity using body composition as measured by dual-energy X-ray absorptiometry in a large sample of twins from the TwinsUK cohort, comparing fecal 16S rRNA diversity profiles with six adiposity measures.

Results
We profile six adiposity measures in 3666 twins and estimate their heritability, finding novel evidence for strong genetic effects underlying visceral fat and android/gynoid ratio. We confirm the association of lower diversity of the fecal microbiome with obesity and adiposity measures, and then compare the association between fecal microbial composition and the adiposity phenotypes in a discovery subsample of twins. We identify associations between the relative abundances of fecal microbial operational taxonomic units (OTUs) and abdominal adiposity measures. Most of these results involve visceral fat associations, with the strongest associations between visceral fat and Oscillospira members. Using BMI as a surrogate phenotype, we pursue replication in independent samples from three population-based cohorts including American Gut, Flemish Gut Flora Project and the extended TwinsUK cohort. Meta-analyses across the replication samples indicate that 8 OTUs replicate at a stringent threshold across all cohorts, while 49 OTUs achieve nominal significance in at least one replication sample. Heritability analysis of the adiposity-associated microbial OTUs prompted us to assess host genetic-microbe interactions at obesity-associated human candidate loci. We observe significant associations of adiposity-OTU abundances with host genetic variants in the FHIT, TDRG1 and ELAVL4 genes, suggesting a potential role for host genes to mediate the link between the fecal microbiome and obesity.
Conclusions
Our results provide novel insights into the role of the fecal microbiota in cardio-metabolic disease with clear potential for prevention and novel therapies.

New Study Links Protein in Wheat to the Inflammation of Chronic Health Conditions


sciencenewsline |  Scientists have discovered that a protein in wheat triggers the inflammation of chronic health conditions, such as multiple sclerosis, asthma and rheumatoid arthritis, and also contributes towards the development of non-coeliac gluten sensitivity.

With past studies commonly focusing on gluten and its impact on digestive health, this new research, presented at UEG Week 2016, turns the spotlight onto a different family of proteins found in wheat called amylase-trypsin inhibitors (ATIs). The study shows that the consumption of ATIs can lead to the development of inflammation in tissues beyond the gut, including the lymph nodes, kidneys, spleen and brain. Evidence suggests that ATIs can worsen the symptoms of rheumatoid arthritis, multiple sclerosis, asthma, lupus and non-alcoholic fatty liver disease, as well as inflammatory bowel disease.

ATIs make up no more than 4% of wheat proteins, but can trigger powerful immune reactions in the gut that can spread to other tissues in the body. Lead researcher, Professor Detlef Schuppan from the Johannes Gutenberg University, Germany, explains, "As well as contributing to the development of bowel-related inflammatory conditions, we believe that ATIs can promote inflammation of other immune-related chronic conditions outside of the bowel. The type of gut inflammation seen in non-coeliac gluten sensitivity differs from that caused by coeliac disease, and we do not believe that this is triggered by gluten proteins. Instead, we demonstrated that ATIs from wheat, that are also contaminating commercial gluten, activate specific types of immune cells in the gut and other tissues, thereby potentially worsening the symptoms of pre-existing inflammatory illnesses".

Clinical studies are now due to commence to explore the role that ATIs play on chronic health conditions in more detail. "We are hoping that this research can lead us towards being able to recommend an ATI-free diet to help treat a variety of potentially serious immunological disorders" adds Professor Schuppan.

Wednesday, October 5, 2016

Obesity genes probably didn't evolve to help us survive famine


physorg |  Genes that helped our ancestors store fat in times of famine may have been useful, but whether they cursed future generations with a predisposition toward obesity is a little more controversial. This popular "thrifty gene hypothesis" has had its critics, but with a study published September 22 in Cell Metabolism, there is now evidence that nearly all the common obesity-related genes show no properties of traits that evolved because they provide an adaptive advantage.

"This is probably the hardest evidence so far against the thrifty gene hypothesis—our ambition here is for people to entertain a wider range of ideas about where the genetic basis of complex diseases, like obesity, comes from," says John Speakman, a biologist at the Chinese Academy of Sciences Institute of Genetics and Developmental Biology in Beijing, who co-authored the piece with Guanlin Wang, one of his PhD students at the Chinese Academy of Sciences. "The process of evolution is a lot more complex than just the spread of favorable traits by natural selection, and the thrifty gene is like an emblem of this older way of thinking about evolutionary aspects of medicine."