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. The gene discussed is CCL2; the disease is gastrointestinal disease.