Strong case for dopamine

This is for hypothesis and even educated speculation.
CirqueduSoleil90
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Strong case for dopamine

Unread post by CirqueduSoleil90 »

Some time ago I took a DNA test and found out I have a gene called gs224 (https://www.snpedia.com/index.php/Gs224). This gene leads to low levels of dopamine. Let's follow the dopamine trail.

There are at least two recovery stories for Inositol, which increases dopamine receptors (https://pubmed.ncbi.nlm.nih.gov/11267629/). I've read about people taking 18g of Inositol a day, but I can barely tolerate a few hundred milligrams. Even at that level I go completely anhedonic. I read somewhere although I've lost the reference, that Inositol initially blunts dopamine release. Perhaps my low initial levels of dopamine make me susceptible to this effect in a way that people without this gene aren't. But that's a side track. Even if Inositol affects dopamine and I apparently have an issue with dopamine, Inositol also has has a host of other effects, any of which might be the real reason for the recoveries. Let's keep digging.

There are also recovery stories for St Johns Wort (SJW) which also increases dopamine (https://pubmed.ncbi.nlm.nih.gov/15148244/). Of course, SJW also has a host of other effects, but at least dopamine is common theme for SJW and Inositol.

There are also recovery stories for various anabolic steroids and subsequent post cycle therapy (PCT). The connection between steroids and libido does not seem to be well understood, but it seems that testosterone does not directly affect libido. Testosterone does however affect dopamine (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3949980/). Now we have three compounds, all with wildly different effects, but with the common denominator that they affect dopamine.

Finally, at least one person has recovered using pramipexol which directly activates dopamine receptors and another using dextroamphetamine, which also activates dopamine receptors. These two last compounds are the clearest link to dopamine since these compounds don't do much except activate dopamine receptors.

The likely culprit: dopamine.
BlackCat
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Re: Strong case for dopamine

Unread post by BlackCat »

Dopamine agonists are known to cause hypersexuality as a side-effect. Dopamine lowers prolactin (a hormone that inhibits sexuality). Whether you have PSSD or not, a drug that increases dopamine is likely to make you more horny.
rmichaelballow
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Re: Strong case for dopamine

Unread post by rmichaelballow »

CirqueduSoleil90 wrote: Thu Jun 23, 2022 2:33 am Some time ago I took a DNA test and found out I have a gene called gs224 (https://www.snpedia.com/index.php/Gs224). This gene leads to low levels of dopamine. Let's follow the dopamine trail.

There are at least two recovery stories for Inositol, which increases dopamine receptors (https://pubmed.ncbi.nlm.nih.gov/11267629/). I've read about people taking 18g of Inositol a day, but I can barely tolerate a few hundred milligrams. Even at that level I go completely anhedonic. I read somewhere although I've lost the reference, that Inositol initially blunts dopamine release. Perhaps my low initial levels of dopamine make me susceptible to this effect in a way that people without this gene aren't. But that's a side track. Even if Inositol affects dopamine and I apparently have an issue with dopamine, Inositol also has has a host of other effects, any of which might be the real reason for the recoveries. Let's keep digging.

There are also recovery stories for St Johns Wort (SJW) which also increases dopamine (https://pubmed.ncbi.nlm.nih.gov/15148244/). Of course, SJW also has a host of other effects, but at least dopamine is common theme for SJW and Inositol.

There are also recovery stories for various anabolic steroids and subsequent post cycle therapy (PCT). The connection between steroids and libido does not seem to be well understood, but it seems that testosterone does not directly affect libido. Testosterone does however affect dopamine (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3949980/). Now we have three compounds, all with wildly different effects, but with the common denominator that they affect dopamine.

Finally, at least one person has recovered using pramipexol which directly activates dopamine receptors and another using dextroamphetamine, which also activates dopamine receptors. These two last compounds are the clearest link to dopamine since these compounds don't do much except activate dopamine receptors.

The likely culprit: dopamine.
What you're seeing here is one part of the way to recover, and that's addressing dopamine. As seen on the thread about cabergoline (a dopamine D2 agonist), and a temporary full recovery (or window), addressing dopamine helps substantially, not just for libido and erectile function, but for sensation as well. But it seems to be a bit more complicated than just agonizing receptor sites, and the entire dopaminergic system as a unit, needs to be restored.

The sex steroid recoveries are interesting. The affect on dopamine that testosterone has, is limited to the state of the dopaminergic system (I believe). Some people do quite well w/ Clomid, and or actual TRT, and managing estradiol, and some do not. The ones that do not, seem to have a more "broken," if you will, dopaminergic system.

But ALL of this plays a role and more. The system of sexual function is too complex to be mediated or controlled exclusively by dopamine. You've got approach every angle. Sex hormones + dopamine, I've seen be a successful route to take, that has landed people in long stints of recovery.

And what's important for people to understand is that merely taking Tyrosine or phenylalanine, both dopamine precursors, isn't going to solve the dopamine issue, if the conversion enzymes and gene regulation of dopamine creation/synthesis are malfunctioning, which I believe is the case in some. Working on up-regulating the expression of Tyrosine hydroxylase, should be one particular target, in these situations. Another would be attempting to restore the way the brain actually makes dopaminergic neurons. We actually have evidence that TH gets down-regulated in the presence of SSRIs. This study (https://pubmed.ncbi.nlm.nih.gov/1977162/) was with long term/chronic use, but who's to say this doesn't happen in shorter term use as well.
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