In the evolution of alcoholic liver disease (ALD), human evidence for the early stages of the disease is lacking while animal studies imply that the gut-liver axis plays a vital role. Patients with alcohol use disorder (AUD) who were enrolled in a recovery program were compared to healthy controls. The researchers measured intestinal epithelial and vascular permeability (IP) (using 51Cr-EDTA urinary excretion, fecal albumin content, and immunohistochemistry in distal duodenal biopsies), epithelial damage (histochemistry, serum iFABP, and intestinal gene expression), and microbial translocation (Gram – and Gram + serum markers by ELISA). 16S rRNA sequencing was employed to assess the microbiota linked with the duodenal mucosa as well as the fecal microbiome. In addition, ALD was staged by serum CK18-M65, AST, and ALT, as well as fibroscan. Only a minority of AUD patients reported elevated 51Cr-EDTA and fecal albumin, as well as impaired tight junctions and plasmalemma Vesicle-Associated Protein-1 expression in the vasculature. The so-called enhanced intestinal permeability was linked to changes in the fecal microbiota rather than changes in the duodenal microbiota or modifications in the intestinal epithelium. Enhanced microbial translocation in AUD patients was not explained solely by a leaky gut. AUD patients with advancing ALD, on the other hand, had duodenal dysbiosis with a change in dominance toward certain possible pathogenic bacteria genera (Streptococcus, Shuttleworthia, Rothia), increased IP, and raised indicators of microbial translocation (steatohepatitis, state-fibrosis). Increased microbial translocation and dysbiosis of the duodenal mucosa are linked to Progressive ALD, even in the early stages of the disease. But an increase in IP is not associated with such variations. Increased IP, on the other hand, appears to be linked to fecal microbiota dysbiosis.