Can statins combat intestinal dysbiosis?
The intestinal flora of obese people taking statins resembles that of non-obese patients. Statins may modulate the gut microbiota, thereby preventing dysbiosis, although no causal link has yet been established.
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From its early days, metagenomic research has sought to understand the links between the gut microbiota and obesity. Since 2012, (sidenote: European project involving over 2,000 participants in good health or at different stages of progression of cardiometabolic diseases (obesity, diabetes mellitus and cardiovascular disease). The participants were recruited in Paris (France), Leipzig (Germany) and Copenhagen (Denmark). www.metacardis.net ) has been studying the potential role of microbiota in the development of cardiometabolic diseases. Its work includes the characterization of the microbiota of 888 obese and non-obese subjects, more than 42% of whom reported taking at least one type of medication. The effects of the most common therapies were assessed, particularly those of statins.
An enterotype marker for inflammation?
Several links were found between obesity markers and gut microbiota in the 782 participants not taking statins. For example, stool softness and inflammation increased with body mass index (BMI), while BMI, body fat percentage and serum triglyceride levels were correlated with changes in the gut microbiota. Most importantly, a link was observed between the prevalence of Bact2 enterotype (high proportion of Bacteroides, low proportion of Faecalibacterium), BMI and inflammation. Thus, while only 3.90% of normal weight and overweight people had this enterotype, this percentage rose to 17.73% in obese individuals. Moreover, the greater the number of Bacteroides, the more acute the inflammation, including among slim people. In addition, the inflammation levels of participants with the Bact2 enterotype were higher than expected based on their obesity status alone, which suggests Bact2 is a potentially dysbiotic enterotype associated with low-grade inflammation.
Effect of statins on microbiota
Conversely, among the 106 participants receiving statins, the prevalence of Bact2 did not increase with BMI: among obese subjects, only 5.88% of those treated with statins had the Bact2 enterotype (vs. 17.73% of obese subjects not treated with statins). This result–confirmed on two separate cohorts–suggests that statins may limit alterations to the intestinal microbiota. Although the study did not establish a causal link between the drug and the lower prevalence of Bact2, two processes, or a combination thereof, may be involved:
• By influencing the growth of certain microorganisms, statins may counteract the role of gut bacteria in patients with inflammatory and metabolic obesity comorbidities
• And/or the anti-inflammatory effects of statins may attenuate the microbiota-host interactions and allow the subsequent development of enterotypes not associated with inflammation
New projects will be launched to verify whether statins have a direct effect on the bacterial flora or whether other factors (such as an improved lifestyle for people with higher awareness of cardiovascular risk) are involved.
