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Mitochondrial dysfunction and insufficient ATP synthesis Mitochondrial dysfunction is one of the most important pathologic hallmarks in CFS, characterized by suppressed mitochondrial respiration, impaired activities of ETC and mitochondrial membrane potential (MMP), and enhanced mitochondrial membrane permeability as a result of elevated levels of pro-inflammatory cytokines (TNF- and IL-1) and increased oxidative and nitrosative stresses, the ultimate result of which could be altered ATP production and mitochondrial shutdown (Morris and Maes 2014)
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That combination (our Wolverine protocol) is our most popular peptide treatment
