About three years ago, this blog looked at the link between gut microbes, diet, genes and heart disease (Linking diet, genes, and gut microbes to…heart disease | gutsandgrowth).
A summary of the most recent information on this topic: H Tilg. “A Gut Feeling About Thrombosis” (NEJM 2016; 374: 2494-6).
Background: Previous research has shown that certain dietary nutrients that include choline are processed by gut microbes to produce trimethylamine (TMA) which is converted into TMA-N-O (TMAO) by the liver. Particular foods that have been associated with higher TMAO include meats and eggs. It has been observed that antibiotics, presumably by their affect on gut microbes, reduce TMAO levels.
What’s new: Zhu et al (Cell 2016; 165: 111-24) “gave mice excess of dietary choline, microbe-generated TMAO enhanced platelet responsiveness in vivo, promoting a prothrombotic phenotype” was blocked by the administration of oral antibiotics. Fecal microbiota transplantation, however, elevated the risk of thrombosis when administered to germ-free mice.
This data shows more clearly a causal relationship between TMAO and thrombotic mechanisms via platelet activation and a causal relationship between gut microbes and TMAO levels. However, this data does not determine exactly how we should modify our diets and or microbes to achieve improved clinical outcomes.