Please let me know if this makes sense. Nitric oxide is potentially mediated by DHT (there is a study on the forum that shows this, but I can’t find at the moment). It seems plausible that when we messed with DHT, we messed with NO levels/NO pathway.
Arginine can either be catabalized by NO synthase (which produces NO), or arginase (which produces ornithine and urea). Apparently, these enzymes compete for Arginine as their target substrate. Many of the post-propecia symptoms may potentially be explained as a result of changing the efficacy of NO synthase to catabalize Arginine.
NO, as we know, is important for blood flow, but also has many other effects in the peripheral and central nervous system. It has been linked to regulation of dopamine and glutamate activity, learning and memory, and sympathetic neural activity. A decrease in NO can lead to an increase in sympathetic activity. This has damaging effects on the body and brain over time, and certainly can lead to erectile dysfunction (as parasympathetic activity is necessary for relaxing smooth penile tissue to initiate and maintain an erection).
If NO synthase is inefficient in binding Arginine, more ornithine and urea should be produced. Ornithine is a precursor to glutamate (major excitatory neurotransmitter). Glutamate is antagonistic to dopamine in many brain regions. A decrease in dopamine has can lead to impairments in movement, and reward pathways.
It might make sense to test levels of ornithine and urea and the metabolites of NO to see if there is an imbalance- I’m not sure if these are typically done in a regular lab. It seams that high levels of nitrites and low levels of Arginase have been linked to schizophrenia and Alzheimer’s.
It might also be a good idea to check global sympathetic activity by checking plasma levels of norepinephrine. An imbalance between neural excitation and inhibition can be checked by means of EEG.
What do you think? Attached are some of the relevant studies.