IL6 and gastrointestinal disease: Mechanisms that have been extensively reported to drive pathophysiologic bone loss in inflammatory hepato-gastrointestinal disease states, including increased liver CXCL1, CCL2, CSF1, IL6 and TNF, upregulated circulating TNF, decreased circulating IGF1, increased marrow TH17 cells/IL17a, unbalanced RANKL:OPG ratio, enhanced osteoclastogenesis, and blunted osteoblastogenesis44, 64–68, are astonishingly the same immunomodulatory mechanisms which appear to mediate the commensal gut microbiota’s catabolic effects on skeletal homeostasis in health.