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More importantly, the dysfunction of Na + /K + -ATPase leads to secondary mitochondrial damage through ion imbalances: intracellular Na + accumulation promotes reverse operation of the sodium-calcium exchanger (NCX), resulting in intracellular calcium overload (85), which is a key potential trigger for mitochondrial structural damage and functional impairment (86)

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This is the active form that can actually fight off free radicals

Excess saturated fatty acid intake, particularly palmitic acid, results in increased ceramide synthesis which has been shown to be both a cause and effector of pancreatic -cell stress resulting in impaired insulin secretion

That same body of work fed into an early-phase human trial registration (NCT02637284) that was later withdrawn before results were reported, which is why anyone telling you BPC-157 is "clinically proven" in humans is overstating the record