It is well known that minoxidil has to be converted to minoxidil sulfate by the SULT1A1 enzyme in order to work as KATP channel (potassium-sensitive ATP channels) opener. Which in turn stimulates hair follicles, albeit through unknown (not exactly known) mechanisms. It is shown that SULT1A1 enzyme activity is a potent indicator of minoxidil’s effectiveness on regrowing hair. Thus the lack of SULT1A1, be it on follicular (hair) regions or liver can both mechanistically (theoretically) and empirically be used to determine an individual’s predicted response to minoxidil over the course of the treatment. Here I propose that liver problems, whether it be in the context of NAFLD or ALD/ARLD, although not definitely, MAY effectively REDUCE an individual’s response to oral minoxidil since oral minoxidil is sulfated through primarily liver. The impairing in SULT1A1 enzymatic function MAY result in a substantial decrease in sulfation of minoxidil to minoxidil sulfate thus reducing the drug’s effectiveness in some cases by more than HALF.
Liver dysfunction may attenuate oral minoxidil efficacy in some individuals via reduced systemic sulfation, but compensatory extrahepatic and follicular sulfation likely limits the magnitude of this effect, I think