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It is not FDA-approved for human therapeutic use, and most evidence involves preclinical studies, animal models, and limited early human safety data

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A study of DNA repair gene polymorphisms (XRCC1 Arg399Gln, XRCC3 Thr241Met XPD Lys751Gln, XPG Asp1104His, APE1 Asp148Glu, and HOGG1 Ser326Cys) suggested that APE1, XRCC1, and XRCC3 genetic variants might be a risk factor for PD by increasing oxidative stress, which might cause the loss of dopaminergic cells in the substantia nigra and locus coeruleus, which could in turn lead to abnormal signal transmission and the development of PD [39]

This is why combining both produces greater than additive effects: they suppress both the homeostatic and the hedonic drives to eat