Gyno from gabapentin, what is going on?

[jJjburton]

Agreed gabaoentin really helps. Fuck Ssris and anti-depressants. Their trash

100%.

 

[Vanargandar]

Man, you're just mixing so many things up, ... There are in essence no newer SSRI's or older ones. All were brought to the market in a similar timeframe. Vortioxetine is not classified as an SSRI, it modulates certain serotonin receptors and also antagonizes SERT at higher dosages, and SNRI's are also not SSRI's; they're SNRI's.

As @Megadick3000 noted, SNRI's are not the first line treatment for anxiety. I personally can't stand elevated NE levels, the feeling I get from them is exactly the same that I have all the time - only potentiated. I know you've read a paragraph somewhere stating that a1a receptor activation in basolateral amygdala facilitates GABA release, but it's far from being so simple. Especially with chronic anxiety, which has chronically elevated NE levels. So be more careful in giving such advice, as somebody might just take your word for it and get a quick and easy panic attack, or something which similarly not a pleasant experience.

What I do agree with you though, is the that pregabalin is not the best anxiety treatment. If excess glutamate is the problem then maybe lamotrigine might help, or maybe helping those underpowered ATP pumps by improving mitochondrial function. Also going keto helps. However, for some, pregabalin works on the long run.

You've got "short allele's"? That's why SSRI's are not working for you?

"Vortioxetine is used to treat major depressive disorder (MDD). It is an antidepressant and belongs to a group of medicines known as selective serotonin reuptake inhibitors (SSRIs). Vortioxetine works by increasing the activity of a chemical called serotonin in the brain."

"Vortioxetine differs from selective serotonin reuptake inhibitors (SSRIs) in its multimodal effect on serotonin transport and reuptake,' said study researcher Roger S. McIntyre, MD, FRCP, a professor of psychiatry at the University of Toronto in Ontario, Canada, and Psychiatry Advisor editorial board member.

'Vortioxetine may also affect a variety of other neurotransmitters. The relevance is that it’s the first antidepressant to affect the domain of cognition independently, a domain we struggle to treat well in depression.'

Vortioxetine received FDA approval for the treatment of major depressive disorder in 2013. The drug is an SSRI, but it also acts as a 5HT agonist, antagonist, and transport inhibitor."

That was a simple Google search, by the way.

I'm fully aware that SSRIs and SNRIs are not the same thing. As far as "newer", I'm referring to SSRIs/SNRIs that were released recently, as opposed to something like Zoloft that was released in 1992.

I also know that SNRIs are not a first line of treatment for anxiety, typically SSRIs are, at least in the US...unless your psychiatrist is willing to prescribe you benzos right from the start, which is highly doubtful. I would be willing to admit that some doctors would be more likely to prescribe something like Buspirone or another anxiolytic before an SSRI, but it also completely depends on the patients severity of symptoms.

I'm just assuming you skimmed over the part where I explained all of this is highly individualistic and he should talk to a medical professional? Because I explicitly stated that. The guy asked a question and I gave him my personal experience and opinion, simple as.

I would, however, agree that Lamotrigine would be more useful as it's prescribed off-label as a mood stabilizer and I currently take that along with my Pristiq as a secondary medication. It would also be worth asking if OP takes a Glutamine supplement, as that can directly increase Glutamate, hence why something like a Lamotrigine could help along with cessation of Glutamine supplementation.

Yeah I have no idea man, I'm not a geneticist. My psych doc ordered a gene test and it showed that I don't respond well to SSRI-classes of drugs, which was blatantly apparent when I (as explained previously) took Lexapro with zero relief of symptoms but had all the bad side-effects.

 

[Jin23]

"Vortioxetine is used to treat major depressive disorder (MDD). It is an antidepressant and belongs to a group of medicines known as selective serotonin reuptake inhibitors (SSRIs). Vortioxetine works by increasing the activity of a chemical called serotonin in the brain."

"Vortioxetine differs from selective serotonin reuptake inhibitors (SSRIs) in its multimodal effect on serotonin transport and reuptake,' said study researcher Roger S. McIntyre, MD, FRCP, a professor of psychiatry at the University of Toronto in Ontario, Canada, and Psychiatry Advisor editorial board member.

'Vortioxetine may also affect a variety of other neurotransmitters. The relevance is that it’s the first antidepressant to affect the domain of cognition independently, a domain we struggle to treat well in depression.'

Vortioxetine received FDA approval for the treatment of major depressive disorder in 2013. The drug is an SSRI, but it also acts as a 5HT agonist, antagonist, and transport inhibitor."

That was a simple Google search, by the way.

Hm, I don't know why you thought this was necessary. It doesn't help your argument. I'm fully aware of vortioxetine's MOA's. I took it twice, so I've studied it enough and have first hand experience. I said it's not classified as an SSRI. If you were trying to argument that statement, you just succeeded in doing the opposite. But I presume you had something other in mind? You were right, however, stating that it's good for treating anxiety. It's an 5HT1a agonist. In short; 5HT1a is the main serotonin receptor responsible for serotonins anxiolytic effects. And that is due to how GABAergic interneurons work and project to pyramidal neurons, causing inhibition or disinhibition.

I know this is an aas board, so a degree of unnecessary hostile confrontation coupled with delusional narcissism is to be expected, but let's not do it. The thing you're doing with the quotes is a bit funny though ... Wrong guy.

So you are on lamotrigine and an SNRI. Interesting. Why are you taking aas? They are totally contraindicated for PTSD and GAD. I mean, they're contraindicated for mental health in general, just the opposite of it, but what you have is exactly the thing that aas directly worsen. Maybe you're being medicated enough for you to be able to pull this off? But even so, aas are gene transcribing altering drugs. Presumably, they change your neurobiology for the worst in the long run. They just might change how your excitatory system works.

Has lamotrigine been helpful on the long run or did you see a reduction in it's effectiveness? Do you also have any executive functions problems? Bc lamotrigine, while lowering excitatory transmission might help with anxiety and mood stabilization, it also lowers cognition quite a bit.

What I said about ATP pumps and mitochondria is actually an interesting topic, or at least the general directions it's pointing at. While the glutamate system is implicated in all manners of psychiatric illness, it's not necessary to target it with drugs. You can try and figure out what's the problem and tackle it there instead of dealing with it at the end off the stick.

 

[jJjburton]

Hm, I don't know why you thought this was necessary. It doesn't help your argument. I'm fully aware of vortioxetine's MOA's. I took it twice, so I've studied it enough and have first hand experience. I said it's not classified as an SSRI. If you were trying to argument that statement, you just succeeded in doing the opposite. But I presume you had something other in mind? You were right, however, stating that it's good for treating anxiety. It's an 5HT1a agonist. In short; 5HT1a is the main serotonin receptor responsible for serotonins anxiolytic effects. And that is due to how GABAergic interneurons work and project to pyramidal neurons, causing inhibition or disinhibition.

I know this is an aas board, so a degree of unnecessary hostile confrontation coupled with delusional narcissism is to be expected, but let's not do it. The thing you're doing with the quotes is a bit funny though ... Wrong guy.

So you are on lamotrigine and an SNRI. Interesting. Why are you taking aas? They are totally contraindicated for PTSD and GAD. I mean, they're contraindicated for mental health in general, just the opposite of it, but what you have is exactly the thing that aas directly worsen. Maybe you're being medicated enough for you to be able to pull this off? But even so, aas are gene transcribing altering drugs. Presumably, they change your neurobiology for the worst in the long run. They just might change how your excitatory system works.

Has lamotrigine been helpful on the long run or did you see a reduction in it's effectiveness? Do you also have any executive functions problems? Bc lamotrigine, while lowering excitatory transmission might help with anxiety and mood stabilization, it also lowers cognition quite a bit.

What I said about ATP pumps and mitochondria is actually an interesting topic, or at least the general directions it's pointing at. While the glutamate system is implicated in all manners of psychiatric illness, it's not necessary to target it with drugs. You can try and figure out what's the problem and tackle it there instead of dealing with it at the end off the stick.

I have read so much of your stuff, how do you know so much? Do you have a degree in the field? Or just reviewed alot of info?

 

[Vanargandar]

Hm, I don't know why you thought this was necessary. It doesn't help your argument. I'm fully aware of vortioxetine's MOA's. I took it twice, so I've studied it enough and have first hand experience. I said it's not classified as an SSRI. If you were trying to argument that statement, you just succeeded in doing the opposite. But I presume you had something other in mind? You were right, however, stating that it's good for treating anxiety. It's an 5HT1a agonist. In short; 5HT1a is the main serotonin receptor responsible for serotonins anxiolytic effects. And that is due to how GABAergic interneurons work and project to pyramidal neurons, causing inhibition or disinhibition.

I know this is an aas board, so a degree of unnecessary hostile confrontation coupled with delusional narcissism is to be expected, but let's not do it. The thing you're doing with the quotes is a bit funny though ... Wrong guy.

So you are on lamotrigine and an SNRI. Interesting. Why are you taking aas? They are totally contraindicated for PTSD and GAD. I mean, they're contraindicated for mental health in general, just the opposite of it, but what you have is exactly the thing that aas directly worsen. Maybe you're being medicated enough for you to be able to pull this off? But even so, aas are gene transcribing altering drugs. Presumably, they change your neurobiology for the worst in the long run. They just might change how your excitatory system works.

Has lamotrigine been helpful on the long run or did you see a reduction in it's effectiveness? Do you also have any executive functions problems? Bc lamotrigine, while lowering excitatory transmission might help with anxiety and mood stabilization, it also lowers cognition quite a bit.

What I said about ATP pumps and mitochondria is actually an interesting topic, or at least the general directions it's pointing at. While the glutamate system is implicated in all manners of psychiatric illness, it's not necessary to target it with drugs. You can try and figure out what's the problem and tackle it there instead of dealing with it at the end off the stick.

Dude, you literally said it's not classified as an SSRI, and a simple Google search showed that it's classified with an SSRI. I'm not sure what you're even trying to argue.

I'm being anywhere close to narcissistic, I'm simply addressing what you responded with, half of which you ignored. You came at me like I was trying to play armchair psychiatrist for this guy, which isn't the case at all, implying my opinion was dangerous. We're on a harm reduction board with people who have varying degrees of knowledge within different niches, I don't remember a disclaimer when signing up stating, "You can only post if you're able to quote PubMed verbatim." So yeah, sorry that myself and others on this board clearly aren't intellectual and scientific juggernauts like yourself.

I am completely aware of the long-term implications of abuse from AAS, however, what would be worse (in your opinion) for long-term neurodegeneration; walking around with sub 125-150 ng/dL Testosterone levels due to clinical hypogonadism or taking 150-200mg of test per week and having a ~500 ng/dL level at 30? I can tell you anecdotally (i.e. means absolutely nothing), I feel like a normal human being on TRT as an adjunct as opposed to standalone psychiatric drugs.

I'm not here to argue with anyone, clearly not you, as you're just going to Ben Shapiro me into oblivion. Like I mentioned, I'm just trying to help OP in whatever way I can. If my advice is shit and doesn't help, I take no offense, no one has to listen to me.

 

[RunTrenFcukTens]

When she’s known for stealing gabs so you have to hold her like this.

 

[Jin23]

Dude, you literally said it's not classified as an SSRI, and a simple Google search showed that it's classified with an SSRI. I'm not sure what you're even trying to argue.

I'm being anywhere close to narcissistic, I'm simply addressing what you responded with, half of which you ignored. You came at me like I was trying to play armchair psychiatrist for this guy, which isn't the case at all, implying my opinion was dangerous. We're on a harm reduction board with people who have varying degrees of knowledge within different niches, I don't remember a disclaimer when signing up stating, "You can only post if you're able to quote PubMed verbatim." So yeah, sorry that myself and others on this board clearly aren't intellectual and scientific juggernauts like yourself.

I am completely aware of the long-term implications of abuse from AAS, however, what would be worse (in your opinion) for long-term neurodegeneration; walking around with sub 125-150 ng/dL Testosterone levels due to clinical hypogonadism or taking 150-200mg of test per week and having a ~500 ng/dL level at 30? I can tell you anecdotally (i.e. means absolutely nothing), I feel like a normal human being on TRT as an adjunct as opposed to standalone psychiatric drugs.

I'm not here to argue with anyone, clearly not you, as you're just going to Ben Shapiro me into oblivion. Like I mentioned, I'm just trying to help OP in whatever way I can. If my advice is shit and doesn't help, I take no offense, no one has to listen to me.

Ben Shapiro what? How old are you?

I am completely aware of the long-term implications of abuse from AAS, however, what would be worse (in your opinion) for long-term neurodegeneration; walking around with sub 125-150 ng/dL Testosterone levels due to clinical hypogonadism or taking 150-200mg of test per week and having a ~500 ng/dL level at 30? I can tell you anecdotally (i.e. means absolutely nothing), I feel like a normal human being on TRT as an adjunct as opposed to standalone psychiatric drugs

TRT? Nobody was talking about trt.

Dude, you literally said it's not classified as an SSRI, and a simple Google search showed that it's classified with an SSRI. I'm not sure what you're even trying to argue.

You're misunderstanding.

 

[Vanargandar]

Not trying to hijack the thread to get into a pissing contest. @hyooge, I hope you can fix your gyno issue along with getting proper relief from your anxiety. I would highly advise talking to a medical professional about your issues and explore different psychiatric drugs with lesser side-effects.

 

[RunTrenFcukTens]

Sit here and take these my boy, it’s going to be ok.

 

[RunTrenFcukTens]

 

[connoristiny]

Dosen't gabapentin help with sleep as well?

 

[hyooge]

So in case anyone has such an issue (I dont mind the hijacking I enjoy the content )

0.5 mg Caber removed all issues it seems.
I will take 0.25mg 1x/week until I can change meds.

Any opinions on this?
I have P5P too but caber solved this very quickly.
Any idea the mechanism?
I am still reading and can't pinpoint exactly how prolactin is raised or if it is a false dopamine precursor....

 

[Jin23]

Any idea the mechanism?
I am still reading and can't pinpoint exactly how prolactin is raised or if it is a false dopamine precursor....

This took 5 minutes, so idk how valid the results are, but it seems that pregabalin does impact the HPTA axis; decreasing testosterone by limiting leydig cell function. The prolactin thing is however really not that surprising. If you lower excitatory neurotransmission, chances are that prolactin is going to increase (due to decreased dopamine as you already figured with a dopamine agonist caber), and this was seen in the last cited study.

The results showed that 4000mg/kg of Pregabalin reduced serum testosterone level while it increased FSH and LH levels (p<0.05). Histological investigations of the testes showed a decline on spermatogenesis chain when Pregabalin doses increased to 4000mg/kg. According to our findings, Pregabalin decreases the concentration of testosterone and the number of spermatogenic and Leydig cells, and increases FSH and LH levels at maximum dose.

Conclusion: We suggest that the Leydig cells with a primary function of secreting testosterone are mildly affected by pregabalin.

Pregabalin decreased testosterone level while FSH, LH and prolactin showed a significant increase.

 

[hyooge]

This took 5 minutes, so idk how valid the results are, but it seems that pregabalin does impact the HPTA axis; decreasing testosterone by limiting leydig cell function. The prolactin thing is however really not that surprising. If you lower excitatory neurotransmission, chances are that prolactin is going to increase (due to decreased dopamine as you already figured with a dopamine agonist caber), and this was seen in the last cited study.

The results showed that 4000mg/kg of Pregabalin reduced serum testosterone level while it increased FSH and LH levels (p<0.05). Histological investigations of the testes showed a decline on spermatogenesis chain when Pregabalin doses increased to 4000mg/kg. According to our findings, Pregabalin decreases the concentration of testosterone and the number of spermatogenic and Leydig cells, and increases FSH and LH levels at maximum dose.

Conclusion: We suggest that the Leydig cells with a primary function of secreting testosterone are mildly affected by pregabalin.

Pregabalin decreased testosterone level while FSH, LH and prolactin showed a significant increase.

Yeah unfortunately I could not find any information on activation of GABA-C which does not seem possible, so it is unexplained.

But yeah prolactin levels rose, I am not sure if using a dopamine agonist may cause a different effect from the pregabalin alone?

I feel quite ok, nothing too different.

Caber surely cannot be used long term so I think I will have to try a new med at some point.

 

[Weedup]

Those studies are made on rats and they use huge doses. The max dose of pregabalin is 600mg day.

But they say something interesting:

"The concomitant administration of vitamin E significantly reduced all the previously mentioned biochemical and hormonal adverse effects caused by pregabalin."

 

[Jin23]

Those studies are made on rats and they use huge doses. The max dose of pregabalin is 600mg day.

This is how you convert dosages between species.


View: https://www.reddit.com/r/NicotinamideRiboside/comments/4jf3gz/converting_mouse_dosages_to_human_equivalent/

 

[Jin23]

Yeah unfortunately I could not find any information on activation of GABA-C which does not seem possible, so it is unexplained.

But yeah prolactin levels rose, I am not sure if using a dopamine agonist may cause a different effect from the pregabalin alone?

I feel quite ok, nothing too different.

Caber surely cannot be used long term so I think I will have to try a new med at some point.

First, you're welcome. Secondly, what are you saying now? Neuroleptics lower excitatory neurotransmission, which can translate to a decrease in dopamine and an increase in prolactin. Thirdly, these drugs apparently also lower testosterone, which will skew the androgens - estrogens balance. So both mechanism lead to Gyno Town ...

 

[connoristiny]

Are there any other adverse side effects from gabapentin?

 

[Dave_24]

"Vortioxetine is used to treat major depressive disorder (MDD). It is an antidepressant and belongs to a group of medicines known as selective serotonin reuptake inhibitors (SSRIs). Vortioxetine works by increasing the activity of a chemical called serotonin in the brain."

"Vortioxetine differs from selective serotonin reuptake inhibitors (SSRIs) in its multimodal effect on serotonin transport and reuptake,' said study researcher Roger S. McIntyre, MD, FRCP, a professor of psychiatry at the University of Toronto in Ontario, Canada, and Psychiatry Advisor editorial board member.

'Vortioxetine may also affect a variety of other neurotransmitters. The relevance is that it’s the first antidepressant to affect the domain of cognition independently, a domain we struggle to treat well in depression.'

Vortioxetine received FDA approval for the treatment of major depressive disorder in 2013. The drug is an SSRI, but it also acts as a 5HT agonist, antagonist, and transport inhibitor."

That was a simple Google search, by the way.

I'm fully aware that SSRIs and SNRIs are not the same thing. As far as "newer", I'm referring to SSRIs/SNRIs that were released recently, as opposed to something like Zoloft that was released in 1992.

I also know that SNRIs are not a first line of treatment for anxiety, typically SSRIs are, at least in the US...unless your psychiatrist is willing to prescribe you benzos right from the start, which is highly doubtful. I would be willing to admit that some doctors would be more likely to prescribe something like Buspirone or another anxiolytic before an SSRI, but it also completely depends on the patients severity of symptoms.

I'm just assuming you skimmed over the part where I explained all of this is highly individualistic and he should talk to a medical professional? Because I explicitly stated that. The guy asked a question and I gave him my personal experience and opinion, simple as.

I would, however, agree that Lamotrigine would be more useful as it's prescribed off-label as a mood stabilizer and I currently take that along with my Pristiq as a secondary medication. It would also be worth asking if OP takes a Glutamine supplement, as that can directly increase Glutamate, hence why something like a Lamotrigine could help along with cessation of Glutamine supplementation.

Yeah I have no idea man, I'm not a geneticist. My psych doc ordered a gene test and it showed that I don't respond well to SSRI-classes of drugs, which was blatantly apparent when I (as explained previously) took Lexapro with zero relief of symptoms but had all the bad side-effects.

Hey man I have similar issues to you and was just prescribed lamotrigine, do you or have you taken it with aas?