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This aligns with a previous report suggesting that increased exposure of hydrophobic amino acid residues tends to boost OHC (Aderinola et al., 2020)

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It means the effect is primarily local concentrated in the GI tract, where the peptide is in direct contact with the tissue it needs to repair

The "Hardware First" model posits that chronic symptoms are not the result of permanent brain death, but of persistent, treatable biological dysfunction