Roxybutin: Ah yes, in regards to NAC and glutathione, what I have heard is that they reduce the amount of disulfiram in the body.
Georgia Hunter: Hey Georgia, how have you been?! thank you for sharing your insights on this! Even if this is hitting protozoa in my case I also think it has to be hitting other underlying things as well. But I do suspect the protozoal infection is the lynchpin in my situation.
I'd be curious as to your take on this particular study. After I first took the disulfiram and it flared all my babesia symptoms, gave me same flare as malarone/coartem/antiprotozoals, I suspected it was hitting underlying protozoal infection. And very very hard! I wanted to see if I could find anything that might explain possible mode of action against protozoa. So I looked up studies involving malaria/disulfiram, and I came across this one, suggests the dsf affects metalloprotein oxgenase process for these organisms and the metal ions they need: https://www.ncbi.nlm.nih.gov/pmc/articles/pmc413130/
I talked to my doc yesterday and mentioned this study. They hadn't heard of it, but when they looked it up they were very surprised at how inordinately effective dsf seemed for malaria at what they called basically "homeopathic" doses! (they were also shocked given its effectiveness as to why it hasn't been more widely adopted as a frontline malaria treatment, I have my guesses!)
"Plasmodium falciparum in culture grows optimally at 3% oxygen. Oxygen levels down to 0.5% still support growth, but anaerobic conditions do not. These findings, and the absence of the Krebs cycle in Plasmodium, suggested that in this organism oxygen may not function in electron transport but rather may act through metalloprotein oxygenases. Tetraethylthiuram disulfide (Antabuse, disulfiram) and its reduction product diethyldithiocarbamate inhibit many metalloprotein oxygenases and have a lipid/H2O partition coefficient and high binding constant for metal ions, favoring selective toxicity to the malaria parasite. These compounds exhibited active antimalarial effects in vitro in concentrations down to 0.1 microgram/ml, the lowest level tested. Tetraethylthiuram disulfide at a level as low as 1 microgram/ml inhibited parasite glycolysis with no effect on glycolysis of normal erythrocytes. Erythrocytes pretreated with this drug at 10 microgram/ml did not support growth of the parasite."