I'm starting to see trends in PSSD genomes, this is one. DBH

Original post by Powers — full self-text recovered from the r.genit.al mirror on 2026-10-07 (the export captured the title only):

Basically I've got a lot of PSSD dutch tests now. The one factor that seems to be common among them is a low dopamine metabolite, Homovanillate.

This is a breakdown product of dopamine. The general consensus of course among everyone is that this means that the dopamine levels are too low. Low HVA must mean low dopamine right?

I've been suspicious of this narrative for a while as PSSD behaves a lot like PFS, and it is my suspicion in one of my many theories that could potentially explain the mechanistic behavior of PSSD that there is a buildup of an intracellular transmitter, or the erasure of a concentration gradient.

For signaling to occur, there has to be a difference. If there is no difference, there is no signal. Biological systems are tuned to operate within a particular parameter of concentrations of things, and if that were deranged too much, I could imagine erasure of signaling occurring. This is what happens with PFS with intracellular metabolite accumulation.

I suspect that the reason that this value is often low is not because dopamine levels are low but rather dopamine metabolism is poor. Dopamine levels might actually be astronomical.

Slow COMT seems to be relatively common among PSSD patients, but there's a mutation now that I've seen show up in genomes too much.

Basically, I keep finding rare, high revel score glitches in Dopamine Beta Hydroxylase.

https://en.wikipedia.org/wiki/Dopamine_beta-hydroxylase

I do not think that this is the magic gene for PSSD, but it has now shown up a statistically anomalous amount to the point where I'm suspicious that it is at least one of the possible glitches that form the family of things that make someone susceptible to PSSD.

For PFS I've isolated these two things like glucuronidation or transport or so on. ABCCs, UGTs, SLCOs etc.

I'm still working on that for PSSD, but if you have a genome and you are a PSSD patient, take a look at this specific gene. I'm curious to see if this is a statistical glitch or a real signal.

I plan on probing this in my own patients by utilizing high dose apomorphine as it is a dopamine receptor agonist without actually being dopamine. Adding more dopamine to the situation likely would make things worse if this theory is the correct one. Apomorphine may "window" someone with this problem. It in no way would be a cure, but simply a probe to give information. But if it does temporarily restore some functionality that would be intriguing. If it does absolutely nothing, that would be useful information as well.

Again I have many mechanistic theories that make sense on paper, but only one of them (maybe) is correct at this time. This was the same for PFS, and it took me quite a while to narrow down which was the mechanistically sound and genetically coherent one. But I do plan on attacking this problem systematically the same way.

Thank you if you are willing to offer this personal information here anonymously.

-Dr. Powers