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When intra-portal insulin levels are increased (e.g., obesity, Cushings syndrome, or due to treatment with glucocorticoids and glucagon-like peptide 1 receptor agonists) or decreased (e.g., malnutrition, anorexia nervosa and type 1 diabetes mellitus), these changes secondarily alter hepatic GH sensitivity resulting in a secondary association with discordant GH and IGF-I levels (e.g., high GH/low IGF-I levels or low GH/high IGF-I levels, respectively)

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What begins as vague fatigue or headaches often reflects a deeper disruption in gut and neuroimmune function driven by hidden biotoxins

Senescent human fibroblasts resist programmed cell death, and failure to suppress bcl2 is involved