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All of us produce GLP-1, which is an incretin hormone that gets released into our bloodstream when we eat

The mechanism is straightforward: GLP-1 RAs enhance glucose-dependent insulin secretion, and stacking that on top of glucose-independent insulin release from exogenous insulin or sulfonylureas removes the glucose-dependent safety brake

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During phase 1, interleukin-1 (IL-1) in the DRG tissue was significantly different in the morphine, 10 g/kg BPC-157, and 20 g/kg BPC-157 groups

Fatigue was the most debilitating symptom I experienced with Hashimotos

Its primary mechanism of action involves facilitating the transport of long-chain fatty acids into the mitochondria for beta-oxidation