The use of the pentose phosphate pathway (PPP), or more specifically the enhancement of PPP flux, to support or treat free radical damage is justified by scientific evidence. The PPP is a critical metabolic pathway in cells that generates NADPH, a reducing equivalent necessary for the regeneration of reduced glutathione (GSH), one of the cell's most important antioxidants. NADPH produced in the PPP is utilized by glutathione reductase to convert oxidized glutathione (GSSG) back to its reduced form (GSH), which directly detoxifies reactive oxygen species (ROS) and protects cells from oxidative damage. This pathway is especially vital in red blood cells, which rely heavily on NADPH to prevent oxidative hemolysis.

Scientific studies have demonstrated that deficiencies in enzymes of the PPP (e.g., glucose-6-phosphate dehydrogenase deficiency) increase susceptibility to oxidative damage due to impaired NADPH production. Conversely, upregulation or activation of the PPP enhances cellular antioxidant capacity and resistance to free radical damage. Research in both cellular and animal models supports the view that modulating PPP flux can influence the outcome of oxidative stress-related conditions. However, it is important to note that "pentose phosphate" itself is not administered as a treatment; rather, the pathway's function is targeted or supported, often by ensuring adequate glucose supply or modulating enzyme activity. Thus, the scientific rationale is strong, but direct clinical interventions specifically targeting the PPP for free radical damage are still an active area of research rather than standard therapy.