Yeah, she knows I'm on Test and Deca. She is actually trying to start doing TRT, so I assume she knows a little bit about them (I know its not good to assume, though.) I believe she went went that because I told her that I was concerned with sexual side effects of SSRI's (which I have experienced before), especially while the missus and I are trying to have another baby and the positive effects remeron has on sleep. I've been sleeping like a big fat retarded baby since I started taking it. What about it rouses your skepticism?
Mirtazapine is actually quite a problematic AD for more then one reason and some psychiatrist are very reluctant to prescribe it. It's very hard to wean off, people literarily taper for a year ... but that is - what it is, and it's not it's mayor problem.
Mirtazapine has 3 primary mechanisms of action. The strongest one is histamine receptor 1 antagonism, this is primarily why you sleep better on it and it's the same mechanism that puts you to sleep when you take Benadryl. This effect goes away in time as H1 receptors desensitize. However, for some people it never goes completely out of the way as the H1 antagonism of mirt is so strong. It's secondary moa is alpha adrenergic 2a antagonism. I'm saying "secondary" because in regards to effects on mood and physiology, this is the strongest mechanism. And it's third most prominent mechanism is the antagonism of two serotonin receptors; the psychedelics receptor 5HT2a and the 5HT2c receptor, which is very active in the fight or flight/stress axis (HPA axis) and it's why mirt stabilizes mood and anxiety over the long term.
Now, what's the problematic part? The a2a antagonism elevates dopamine (DA) and noradrenaline (NE) levels, a lot. Also the 5HT2c antagonism helps in this regard. This will elevate your blood pressure, which is problematic if you are cycling, but the more problematic thing is that this can lead to a host of mental problems as you are elevating your catecholamines, constantly. The feedback mechanism by which brain lowers NE release is a2a agonism via NE and this pathway is now severely blocked (depends on the dosage) which can lead to a host of issues. This is very similar to yohimbine, it does the same thing. I remember my psychiatrist telling me a story, how he saved a girls life one time by putting her off mirt.
The H1 antagonism is also very problematic from a metabolic standpoint. You'll probably gain weight, most do. And insulin resistance can become a problem. You'll be hungry all the time. 5HT2c antagonism also plays a role in hunger but H1 antagonism is the bigger problem. Mirt would have been an interesting choice if it wasn't for the stupidly strong H1 antagonism. There is no reason for such strong action on this system and is more or less an unwanted action of the antidepressant (as is with most AD's that have A1 antagonism).
Why I'm skeptical of mirt alongside aas is because of it severely upregulating DA and NE both of which are already elevated on cycle in is one of the primary reasons why aas are problematic, in regards to mental health. Ie. you don't need more DA and NE while on cycle, you actually need an attenuation of DA and NE signaling, either allosteric or mild antagonism.
The good thing about mirt is that it is anti-inflammatory and it does regulate the HPA axis, however, the a2a antagonism is problematic and once the H1 receptors desensitize or multiply (or what ever exactly happens) you'll be left with a lot of stimulation. So tread carefully, do not go above 15mg, or better yet, don't go over 7.5mg until you don't feel the sedating side effects any more. Evaluate your sleep and mood at that point and if all is fine, wait a few weeks and then up the dose.
That being said, mirt is the last thing I'd use on cycle. But if you'd want to go a similar route, without all the sides and problems that mirt has, agomelatine is the much safer choice and if sleep is an issue then add a dual orexin antagonist and you've basically got a fancy variant of mirt, without all the sides and you won't even know you're taking anything.
However, the best choice for aas are still serotonin elevating AD's and or mood stabilizers like lamotrigine, valproate and/or even never AP's like cariprazine. However, in regards to ssri's fluvoxamine is a very anti-inflammatory option. But, from my experience, I'm just trying out agomelatine at a relatively small dose 12.5mg, and I'm very surprised how effective such mild HT2c antagonism in reality is. It's seriously relieving stress and besides some hunger and a bit more fragmented sleep, there is no feeling of actually being on something. But again, for androgens, having extra serotonin is a must, it relieves all the aggression, makes you a lot more peaceful ...
In short, I know this post is big mess, for on cycle support you need to:
- alleviate HPA stress, this can be done either via HT1a or HT2c
- induce hippocampal neurogenesis
- lower dopamine neurotransmission
- also blocking AR expression in the brain is not such a bad idea. Valproate does this.
Imo this are the most important steps. However, we are so individual in how we react to drugs that everybody will find what works best for them. Me personally, I can't stand SSRI's, the brain fog I get from them defeats all the positives, but somebody else might be just fine and blessed be those people, as I love how pleasant and care free SSRI's make me, and high serotonin coupled with high androgens is superman mode switched to ON. You feel strong and confident but at the same time ambivalent and just don't give a fuck.
I don't know what I'm writing any more, ... just be careful with mirt. Go slow.
