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Although additional studies are required to clarify the molecular mechanisms responsible for hyperhomocysteinemia-induced vascular disorders, there is evidence that the direct cytotoxicity of markedly elevated homocysteine and/or of its oxidized by-products (homocysteine thiolactone, homocysteine sulfinic acid, and homocysteic acid) damages endothelial cells (Dudman et al, 1991
Phase 2 studies with GS-9674 are ongoing in patients with NASH (NCT02854605), primary biliary cholangitis (PBC), and primary sclerosing cholangitis (PSC)
Improved athletic performance
Many patients report that appetite suppression makes adherence to nutrition goals feel less like willpower and more like genuine preference change
P-values 0.05 were considered statistically significant
