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The fears are based on mechanism and animal data, not observed human cancer cases simply because BPC-157 hasnt been studied in humans long enough or in enough people to see those outcomes
The conclusion was further validated by terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) and H&E staining (Fig
Nat Med 17(11):14811489
The reason has been ascribed to loss of proteasome activity over time
Reducing mechanical load on compromised joints while using BPC-157 to support tissue repair is a more complete approach than either intervention alone
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