Gut bacteria can be the cause of abdominal fat gain and metabolic disease and are determined by both lifestyle and genetics


  • In the last few years scientists have found that having the wrong kind ion bacteria in your gut can make you fat and can increase the risk of metabolic and heart disease, by metabolising the food we eat and by secreting chemicals which cause inflammation, risk of obesity etc.
  • Now in a new study published recently it was found that what kind of gut bacteria we have and we accumulate depends to a large extent on our genetics. This means that the composition of our gut bacteria is indirectly «inherited» by our parents – but of course it can also be improved  or worsened by food and lifestyle.
  • In this study it was also found that bacteria can actually metabolic fat into sugars by a recently discovered process called glyoxylation. In fact, glyoxylate has been recently described as a risk marker for diabetes.
  • Bacterial diversity, which may be damaged by antibiotics, has a protective effect against obesity and metabolic disease. on the other, healthy foods and low fat low sugar diets can improve the composition of gut bacteria.
  • Oscillospira family bacteria in the gut have been found to have a strong association with abdominal obesity, while christensenella bacteria have been found again to have an anti-obesity effect
  • Source: Heritable components of the human fecal microbiome are associated with visceral fat
  • Abstract: Background. 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.


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