The irreproducibility of preclinical, biomedical research is becoming increasingly problematic, as recently highlighted by Omary et al,1 in the June issue of Gut. As discussed, variations in study design, mouse strain, sex and age are important factors that should be adequately described to promote study reproducibility.1 In line with recent speculation,2 authors also emphasised the gut microbiome as a potential confounder underlying inconsistencies in preclinical research data.
Recently, there has been a large influx of studies reporting dysbiotic changes in many preclinical models of human disease, both GI and non-GI.34 Although informative, much of this research continues to be associative. To dissect causative disease mechanisms, the impact of benign environmental factors relating to study design and rodent husbandry must be acknowledged.
Based on twin studies,5 it is understood that a core subset of bacteria are hereditary.
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