Okay, everything you’ve described changes the situation somewhat.
First, I want to explain why I need all this information. Usually, libido is affected either by hormonal factors or neurochemical ones. You could call it neurohormonal to simplify things, but I separate them so we can understand that there are relatively “coarse” mechanisms of influence and more subtle ones. The first category is something we can determine fairly accurately through bloodwork. The second is our neurotransmitter balance — something we can’t really measure because it’s too complicated outside a scientific laboratory and complex experiments. We can only make indirect assumptions and try to change something experimentally, then wait for some “magic” changes and observe the effects. And what any psychiatrist does is essentially this kind of “magic” manipulation of your brain. If you felt relief, then why it happened matters much less than the fact that it worked. That’s how psychiatry works. And you shouldn’t go into this crystal house with a hammer in your hands, if you understand what I mean.
What I’m getting at is that I don’t see anything in your bloodwork that we could potentially work with to change the situation. Maybe the guys here can suggest something else.
But as far as things outside psychiatric medications that could potentially be looked at or added, there are only a few options that, purely hypothetically, might affect the situation.
- Add HCG 250 IU three times a week. For some people, this helps specifically with libido while on cycle or TRT. There are some hypothetical reasons why this might work.
- Add Proviron 50–100 mg per day. This is obviously a fairly crude approach, simply because Proviron is one of the compounds structurally closest to DHT. Maybe it will work, maybe it won’t. Whether it could make things worse alongside all the psychiatric medications you’re taking is difficult to say. You could ask your psychiatrist for their opinion, because ANY anabolic steroid can enter the brain and have some degree of activity there.
But changing the course of treatment prescribed by your psychiatrist is definitely not something you should do in this case — you’re absolutely right about that. And I don’t want to go into a crystal house with a hammer. So let’s do this: I’ll simply explain my rough logic, which you can discuss with your doctor. I’ll say right away that I don’t currently have all the information — for example, which other medications have been tried and what results they produced. That’s also important, because it’s through experience and experimentation that we can try to find answers.
- Ask your psychiatrist why exactly quetiapine was prescribed and what role they believe it serves. If it’s only about sleep, there are medications that also work through histamine receptors without affecting the dopamine system. And in general, H1 receptor blockade isn’t necessary for improving sleep. For example, DORA-class medications are increasingly entering clinical practice and preserve the natural architecture of sleep better. If we’re talking about signs of bipolar spectrum disorder, then it’s unclear why the dose is only 150 mg. Usually, that’s a starting dose and it’s increased afterward if it’s well tolerated. If you clarify this point, it would be useful information.
- Anxiety is suppressed through serotonin — that’s a fact of clinical practice. But at the same time, you were prescribed bupropion, which acts primarily through norepinephrine and dopamine. It’s often added when there’s insufficient energy, motivation, anhedonia, or sexual side effects. Perhaps your doctor added bupropion specifically for this reason, although that doesn’t necessarily mean it worked.
Now I’ll explain a little about serotonin. Serotonin itself, which is increased by 50 mg of sertraline, acts on a number of serotonergic receptors. Interaction with each of them produces different effects. One of the main mechanisms involved in reducing anxiety is interaction with 5-HT1A receptors.
When talking specifically about serotonin-related suppression of libido and sexual function, 5-HT₂A and 5-HT₂C are of particular interest, as well as 5-HT₃ in some components of sexual dysfunction. By increasing overall serotonergic transmission through SERT, sertraline may increase signaling through 5-HT₂A/5-HT₂C and thereby reduce libido, impair arousal, and especially delay orgasm/ejaculation.
So in theory, your doctor could consider switching sertraline to something else that would sufficiently activate 5-HT1A while blocking 5-HT₂A and 5-HT₂C receptors — for example, mirtazapine. Again, this isn’t a call to action, but rather a suggestion to discuss it with your doctor and ask for their opinion.