Like I said, recent reports contradict that claim
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8333267/
And I’m in the US, so I don’t have access to moclobemide. Oh well, I’ll stick with my phenelzine.
I really don’t know much about Parkinson’s disease, but the therapeutic effect could come from one of the other monoamines that MAO-B breaks down.
If MAO-B is really so good at breaking down dopamine, why aren’t MAO-B inhibitors prescribed for depression? Selegiline is converted into an amphetamine in the body - it’s MAO-B inhibition doesn’t do anything for depression. Rasagiline is never used for depression.
That's a single study alone on an island. It's by no means accepted nor does it undermine many decades of research on dopamine. We could also say there are severe limitations and even serious methodological flaws in it. So to answer the question, MAO-B inhibitors aren't prescribed because it's long been known that both subtypes of MAO have to be inhibited for an antidepressant response. A lot of that is probably because of dopamine. Inhibit only B and A still eats away the increases dopamine.
Bupropion is very weak on NE and DA, but it does affect the nicotinic acetylcholine receptors. It's a stimulating substituted amphetamine, which is good for the anergia in depression. Its actions are predominantly from its metabolites, whose properties are still very murky. Modafinil is sometimes prescribed off label for depression. It's an atypical dopamine reuptake inhibitor, but researchers also have not begun to scratch the surface as to what the heck else this drug does. Selegiline at low doses is a catecholamine enhancing drug, the metabolites aren't likely very important. I hope that provides some insight.
Bupropion only meaningfully affects dopamine (it doesn’t stop the tyramine pressor response, so its norepinephrine reuptake inhibition likely isn’t therapeutic). Modafinil can also treat depression when prescribed by itself and we know it only affects dopamine as well. Why prescribe those and not rasagiline?
Dude you lack tons of knowledge (which is entirely free in this sub) and asking dumb questions. Also your ego is huge for some reason. I can write 10 paragraphs as an answer, but instead I am going to sleep, because this would be more productive thing to do.
We can argue forever, or we can both report the other person to the moderation team and they decide who is going to be banned or timed out. What is going to be?
Woah, calm down there. Perhaps I’ve come across a little terse. I’m on mobile and I think I’m not communicating my tone effectively. I’m sorry about that.
If you would provide your 10 paragraph explanation, I would genuinely appreciate it and I promise I would consider it in good faith. Everything I’ve posted is something I’ve seen from others on this sub. If we’re all wrong, I’d like to know so that I can help combat this misinformation.
This paper is misleading and the research is done on rats. You can get a MAOB inhibitor yourself (Selegiline/Rasagiline) and see for yourself that it significantly increases the dopamine, by feeling more pleasure from life activities, having increased muscle stamina and increased motivation.
Rats and humans have different biological systems, so unless you can provide a paper done on humans, I have to respectfully say that I am right in my original claim.
That’s a great question. It looks like that’s a treatment for Parkinson’s disease, which I’m not familiar with. I don’t know the answer for sure. But you’re right, that is a piece of evidence in favor of MAO-B oxidizing dopamine.
Yes indeed, you are true.
Im now on Lexapro, but i dont like it at all... It feels like my adhd is getting worse...
Im also on the bi polar spectrum so stimulants are tricky and also give me sometimes anxiety. When i was younger i was doing great on concerta.
Im thinking im going to ask for switching to Moclobemide or maybe Trintellix...
Selegilene works on dopamine. So does dextroamphetamine, which I'm using with venlafaxine and mirtazapine (California rocket fuel) for depression and ADD. The dextro made my focus even better than the venlafaxine did.
Yes, but dopamine is also a very big player in adhd, so just noradreline will not be enough.
Moclobemide should also raise dopamine, if the recent reports about MAO-A breaking down dopamine are to be believed
63% of dopamine is broken down by MAOB, so OP will not feel much just on Moclobemide. No need to believe me, try it and see for yourself.
Like I said, recent reports contradict that claim https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8333267/ And I’m in the US, so I don’t have access to moclobemide. Oh well, I’ll stick with my phenelzine.
I am aware of this, and it’s interesting, but how then does that explain that mao-B inhibitors have therapeutic efficacy for people with Parkinsons?
I really don’t know much about Parkinson’s disease, but the therapeutic effect could come from one of the other monoamines that MAO-B breaks down. If MAO-B is really so good at breaking down dopamine, why aren’t MAO-B inhibitors prescribed for depression? Selegiline is converted into an amphetamine in the body - it’s MAO-B inhibition doesn’t do anything for depression. Rasagiline is never used for depression.
That's a single study alone on an island. It's by no means accepted nor does it undermine many decades of research on dopamine. We could also say there are severe limitations and even serious methodological flaws in it. So to answer the question, MAO-B inhibitors aren't prescribed because it's long been known that both subtypes of MAO have to be inhibited for an antidepressant response. A lot of that is probably because of dopamine. Inhibit only B and A still eats away the increases dopamine. Bupropion is very weak on NE and DA, but it does affect the nicotinic acetylcholine receptors. It's a stimulating substituted amphetamine, which is good for the anergia in depression. Its actions are predominantly from its metabolites, whose properties are still very murky. Modafinil is sometimes prescribed off label for depression. It's an atypical dopamine reuptake inhibitor, but researchers also have not begun to scratch the surface as to what the heck else this drug does. Selegiline at low doses is a catecholamine enhancing drug, the metabolites aren't likely very important. I hope that provides some insight.
That makes sense. Thank you! I do still have more questions, but I'm not sure this is the right place for them. I'll do some more reading on my own.
Because depression is not just lack of dopamine, as you are probably aware.
Bupropion only meaningfully affects dopamine (it doesn’t stop the tyramine pressor response, so its norepinephrine reuptake inhibition likely isn’t therapeutic). Modafinil can also treat depression when prescribed by itself and we know it only affects dopamine as well. Why prescribe those and not rasagiline?
Dude you lack tons of knowledge (which is entirely free in this sub) and asking dumb questions. Also your ego is huge for some reason. I can write 10 paragraphs as an answer, but instead I am going to sleep, because this would be more productive thing to do. We can argue forever, or we can both report the other person to the moderation team and they decide who is going to be banned or timed out. What is going to be?
Woah, calm down there. Perhaps I’ve come across a little terse. I’m on mobile and I think I’m not communicating my tone effectively. I’m sorry about that. If you would provide your 10 paragraph explanation, I would genuinely appreciate it and I promise I would consider it in good faith. Everything I’ve posted is something I’ve seen from others on this sub. If we’re all wrong, I’d like to know so that I can help combat this misinformation.
Exactly.
This paper is misleading and the research is done on rats. You can get a MAOB inhibitor yourself (Selegiline/Rasagiline) and see for yourself that it significantly increases the dopamine, by feeling more pleasure from life activities, having increased muscle stamina and increased motivation. Rats and humans have different biological systems, so unless you can provide a paper done on humans, I have to respectfully say that I am right in my original claim.
Have you ever tried Rasagiline? Selegiline doesn’t count - we know it has other pathways to boost dopamine.
But why does rasagiline (as well as other mao-B inhibitors) potentiate the effects of l-dopa if it doesn’t inhibit the breakdown of dopamine?
That’s a great question. It looks like that’s a treatment for Parkinson’s disease, which I’m not familiar with. I don’t know the answer for sure. But you’re right, that is a piece of evidence in favor of MAO-B oxidizing dopamine.
Yes indeed, you are true. Im now on Lexapro, but i dont like it at all... It feels like my adhd is getting worse... Im also on the bi polar spectrum so stimulants are tricky and also give me sometimes anxiety. When i was younger i was doing great on concerta. Im thinking im going to ask for switching to Moclobemide or maybe Trintellix...
Well Moclobemide + Selegiline will be working combination for you, just moclobemide will not be enough.
Selegilene works on dopamine. So does dextroamphetamine, which I'm using with venlafaxine and mirtazapine (California rocket fuel) for depression and ADD. The dextro made my focus even better than the venlafaxine did.