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BPC-157 might be signaling the body to initiate these profound repair processes, but if the underlying cellular energy is depleted, the response could be sluggish or incomplete

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Third, as we will detail below (see Potential Pathogenic Mechanisms of Hyperhomocysteinemia), our own work (Durand et al, 1997a) and the work of Lentz et al (1996) and Bellamy et al (1998) give experimental evidence that moderate hyperhomocysteinemia, which leads to vascular dysfunction, might increase the cardiovascular risk independently of other risk factors

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