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JJ17

Zyprexa vs Risperdal for OCD

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On 15-11-2018 at 12:01 AM, JJ17 said:

Makes sense for the most part. I just don’t like the idea of increasing dopamine as almost any dopamine boosting agent (even simple l-tyrosine) worsened OCD/obsessions for me.

Which dopamine does play a key role in obsessions/addictions, at least of the major known chemicals. 

Today I am trying day 1 of Risperdal so how see how it goes. 

Interesting topic, keep us posted!

I'm still in the process of trying out clomipramine, but I have the feeling that I need something to help it work. Not all the time, because I made progress since being on it but I can relapse for a few hours (or sometimes days) and after that start over again. 
My ocd centers around 'not wanting to think it' and every time I do think it (I'll 'it' explain later) it makes it worse. I keep giving attention to this unwanted thought (as in: disappointed with myself for thinking it). I have the classic 'pink elephant' or 'white polar bear' problem. It's a little similar to body focused obsessions.

I was hoping that there's a med (like an AAP) that could help. I've had lots of help from this forum and especially Browri, but I have an extremely careful pdoc....

 

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On 11/14/2018 at 6:01 PM, JJ17 said:

Makes sense for the most part. I just don’t like the idea of increasing dopamine as almost any dopamine boosting agent (even simple l-tyrosine) worsened OCD/obsessions for me.

Which dopamine does play a key role in obsessions/addictions, at least of the major known chemicals. 

Today I am trying day 1 of Risperdal so how see how it goes. 

Remember that AAPs can modulate dopamine signaling, but they don't increase dopamine levels. Supplements like L-tyrosine are dopamine precursors and encourage your body to make more dopamine. Yes, this certainly could be a problem, but making proper use of your body's existing dopamine supply is a bit different.

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I have tried a LOT of medications for my severe OCD (obsessive thoughts and compulsive rituals).......I have tried various SSRIs at high doses, Abilify, Risperdal, Thorazine, Seroquel, and high dose clomipramine (250mg).

The latest one I tried was Abilify at 15mg (tried for 4 months), and former pdoc took me off that because he said it didn't seem to be doing much.

So far, nothing has worked for my OCD, I am very treatment resistant.....I still suffer greatly from it.

I am seeing a new pdoc next week.......I hope she has some fresh ideas.......Still have hope that something will work.

@JJ17, I hope you will find something that helps you.......

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On 11/16/2018 at 6:26 AM, browri said:

Remember that AAPs can modulate dopamine signaling, but they don't increase dopamine levels. Supplements like L-tyrosine are dopamine precursors and encourage your body to make more dopamine. Yes, this certainly could be a problem, but making proper use of your body's existing dopamine supply is a bit different.

From what I read online in Google search the first result reads:

“Risperidone works in the brain, where it affects various neurotransmitters, in particular dopamine and serotonin (5HT). ... Risperidone works by blocking the receptors in the brain that dopamine acts on. This prevents the excessive activity of dopamine and helps to control schizophrenia.Jul 11, 2012

Risperdal (risperidone) - NetDoctor “ 

 

Also it seems like the majority of them all say it decreases dopamine activity, as excessive dopamine activity or signaling (or whatever the proper terminology is) is believed to cause pyschosis/etc. 

Now I’m not interested in it’s anti-psychotic effects rather if it’s method of action will have an affect on OCD. 

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Wow so I’ve Been on it for a little over a week, or 8 days. 

The first few days I felt like it was having anti-depressant action, oddly enough. Along with anti-OCD action. It did make me tired, and the first few nights I woke up refreshed... 

But then I got too “cocky” and decided why not try to FACE my ocd problems? Not a good idea. Especially EXTREMELY deep rooted ones like mine, they are so deep rooted that’s why I’m forced to try a cocktail (on Zoloft + mirtazapine + Clonzepam + Risperdal) and even with all these meds I still feel it strongly.

BUT.... I think I was able to handle it better then before... I think. Love attachment can be really extreme. I really should have NOT tried to overcome it within the first few days of being on Risperidone ....  Either way I didn’t feel “as bad” and was able to get my mind to focus on something else such as video games. So I guess so far I have been doing better but damn I wish I didn’t dive head first into trying to overcome it so soon. 

So because of that I cannot really say for certain how well it has been for OCD in 8 days as I stupidly tried to tackle it too soon. 

Side effect wise almost nothing besides sleep issues. It seems like it reduced sleep quality as often times when I lay down I find I am constantly moving around trying to get comfortable - which is not normal for me. Normally I either pass out cold or flat out can’t sleep and remain awake. But the restless feeling/tossing in bed is more of a “I am tired and drowsy but can’t get comfortable feeling”. Not sure how long it last. This includes the restless leg feeling sometimes when trying to sleep: which I HATE the RLS feeling. 

I have heard that less dopamine can cause RLS. So could be from the dopamine blockage. 

Otherwise I haven’t noticed any other side effects. Just some sleep issues really and I was expecting it to have a lot more side effects. My body must be used to meds by now or something.  

I’ll update later in say a week or so to see how it’s doing for OCD. 

Edited by JJ17

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Antipsychotics do reduce dopamine signaling but they don't necessarily reduce dopamine levels. In fact, your brain compensates for dopamine blockers by releasing more dopamine. There's a dopamine blocker in the way so it doesn't make a ton of difference what your brain does at that point, but that is how it works.

Less dopamine doesn't necessarily cause RLS. What causes symptoms like restlessness/akathisia are when dopamine signaling is lower than acetylcholine signaling. This is why they give anticholinergics to people with restlessness from antipsychotics. The unfortunate side effect is cognitive dysfunction because acetylcholine is intrinsic to cognition.

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Reading through this thread again, I keep seeing Abilify being mentioned. In my opinion and experience, Abilify is not a good fit for OCD because it tends to increase anxiety and anxiety is the root of OCD. Abilify has done nothing for my OCD. Of course, it depends on the person. It's a strange drug in that some it sedates and others it activates. I believe the chance of activation is greater than sedation. As always though, YMMV.

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Totally off topic but I think Risperidone makes pot much more crazy lol. 

 

Or also/and/or since this is the longest period I have ever taken SSRIS, about 1 year or so. I remember Paxil + pot was pretty nuts. Felt like my serotonin sky rocketed, among who knows what else. Lol. Now a year on that + or other SSRIS. hmm. Or a combo of the SSRI + risperidone is just a heck of a combo.

I happen to live in one of those states where it’s legal, so yeah lol. I’m soooo... why can’t we always feel this good? 

I’m eating Claw chowder and I don’t know why **Clam

Edited by JJ17

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I could have a mild/moderate cause of serotonin syndrome and just not even care lol. 

I cannot stop moving for the life of me. My muscles are going crazy. But I feel absolutely lovely, mentally. 

Ok now I cant stop moving... Sorta....Now I stopped. Uh, well that was fast. 

Feels like maybe blood pressure/etc increased and even anxiety - but not anxiety. It’s weird as hell. The normal butterflies I would normally get are overwhelming. I feel zero of that. None, nada. So...I’m just going to move on

Oh I forgot I took 100mg 5HTP today. No wonder this feels like having super high serotonin... just happy and not giving a damn. Dopamine and noradrenaline give me energy/anxiety and motivation. I have motivation I guess but feel almost a happy numbing? Cause I just like everything I think. 

Oh I don’t recommend marijuana btw... I bet if I turned off the lights I probably could have minor visual hallucinations... I’m going try... come back in a minute...

 

okay I spent what felt like 30 mins insanely high felt like my 3rd eye was opening lol. I’m going to stop typing now 

i like clam chowder and music 

oh and I shattered my phone. Oops 

Edited by JJ17

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On 12/1/2018 at 2:06 AM, JJ17 said:

I could have a mild/moderate cause of serotonin syndrome and just not even care lol. 

I cannot stop moving for the life of me. My muscles are going crazy. But I feel absolutely lovely, mentally. 

Ok now I cant stop moving... Sorta....Now I stopped. Uh, well that was fast. 

 

You would know if you had serotonin syndrome. It sounds like you are experiencing Akathisia, where you feel compelled to constantly move. It is very uncomfortable.  There are several meds that treat Akathisia: propranolol and Cogentin to name a few. You need to call/contact your doc as Akathisia tends not to go away without some form of intervention.

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On 12/1/2018 at 3:33 AM, JJ17 said:

Totally off topic but I think Risperidone makes pot much more crazy lol. 

I've always found this to be the case since starting to take AAPs. Pot is definitely more intense. Makes for a lot of calming dopamine release between an AAP and cannabis

1 hour ago, notloki said:

You would know if you had serotonin syndrome. It sounds like you are experiencing Akathisia, where you feel compelled to constantly move. It is very uncomfortable.  There are several meds that treat Akathisia: propranolol and Cogentin to name a few. You need to call/contact your doc as Akathisia tends not to go away without some form of intervention.

This does sound more like akathisia for sure. Curious. Does it seem to "calm down" when you smoke? Are you able to sit still more? This may reinforce the akathisia theory. One of the components in cannabis, cannabidiol, is a negative allosteric modulator of acetylcholine receptors which may assist with restlessness.

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On 11/23/2018 at 5:19 PM, jt07 said:

Reading through this thread again, I keep seeing Abilify being mentioned. In my opinion and experience, Abilify is not a good fit for OCD because it tends to increase anxiety and anxiety is the root of OCD. Abilify has done nothing for my OCD. Of course, it depends on the person. It's a strange drug in that some it sedates and others it activates. I believe the chance of activation is greater than sedation. As always though, YMMV.

I take Abilify as an augmentation to Effexor for OCD, after dropping Risperidone.

I would say that Risperidone has a more calming effect rather than an energising effect as with Abilify.

On the other hand it is an inverse agonist of the histamine H1 and it hits the receptor pretty hard. This can be very sedating for some. I used to take .5 Risperidone a day and waking up in the morning became *extremely* hard.

They both did the job for me, despite different mechanisms.

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On 12/2/2018 at 9:47 AM, browri said:

I've always found this to be the case since starting to take AAPs. Pot is definitely more intense. Makes for a lot of calming dopamine release between an AAP and cannabis

This does sound more like akathisia for sure. Curious. Does it seem to "calm down" when you smoke? Are you able to sit still more? This may reinforce the akathisia theory. One of the components in cannabis, cannabidiol, is a negative allosteric modulator of acetylcholine receptors which may assist with restlessness.

So does the Risperidone enhance THC? I thought they would only “compete” against each other since the risperidone blocks dopamine or multiple subtypes of it. I linked the picture a couple of pages ago. 

So from what I gather it’s (Risperdal) a very strong D2 blocker, among many others for dopamine and serotonin. Sertonin According to Wikipedia it’s actuallt more potent at 5T2A (0.17 nM) while it’s D2 action is (3.57). 

So since risperidone is “blocking dopamine” does that in turn make dopamine release more effective or sensitive to marijuana? Heck with the whole auto-receptors and pre/post synaptic receptors it gets confusing.

 

Wikipedia states:

“”Risperidone has more pronounced serotonin antagonism than dopamine antagonism”  which is interesting. I guess I’m just confused as to why being a sertonin blocker at multiple other areas (some very potent some less) would benefit OCD? As from what I understand they in general “reduce dopamine activity” or “stabilize it” or what not, as I know by blocking it can actually caused enhanced _____ and so fourth. Very Complex. But still in general wouldn’t something like haloperidol (which seems to be mainly a potent dopamine blocker) be more effective in treating anxiety and OCD compared to risperidone? Since Risperidone claims that be being a Dopamine antagonist (primarily D2) it leads to “reduced dopamine activity/signaling” which is how the medication works - primarily. But since it also blocks multiple sertonin areas it technically reduces sertonin activity. 

While SSRIS “increase activity” (post wise I believe) or whatever the proper wording is. Point being is it seems to me like risperidone is almost doing the opposite of what SSRIS are suppose to do, no? If so wouldn’t that be counter-productive for OCD/anxiety by blocking sertonin when taking risperidone? It seems that haloperidol is not only a much weaker sertonin blocker, but also seems to hit less sertonin areas? So I wonder if that’s true if meds like haloperidol may be better to combine with an SSRI then Risperidone? Since haloperidol doesn’t block nearly as much sertonin as risperidone? 

Maybe someone here knows  

Edited by JJ17

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Maybe you're right and you had to wait a little longer with facing your OCD issues. On the other hand, don't be too hard on yourself. You tried and you might succeed next time!

Keep up posted, I'm really interested in how you're doing on risperidone.

Edited by Catwoman

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@JJ17

I'm no expert but I have been looking into this technical meds stuff out of interest.

Some points to take into account:

* Not all serotonin receptors are "good". 5HT2C for example inhibits dopamine and noradrenaline release, so being a serotonin 5HT2C antagonist like Risperdal is, may be a good thing.
(Actually, it is an inverse agonist on this receptor, which can be oversimplified as "more antagonist than antagonist")
This is also the reason that Prozac is different from other SSRIs, being a 5HT2C antagonist, increasing N/D activity.

* Blocking of 5HT7 reduces anxiety (again, Risperdal is an Inverse agonist on this one too)

* Some receptors are also present on the same firing neuron and function as auto-receptors that are sort of a "braking" system, so antagonising dopamine D2 auto-receptors can increase neurotransmitter activity by releasing more dopamine (Risperdal, again).

* Serotonin 5HT2A has properties that contribute to psychosis.

Edited by HydroCat

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6 hours ago, JJ17 said:

So does the Risperidone enhance THC? I thought they would only “compete” against each other since the risperidone blocks dopamine or multiple subtypes of it. I linked the picture a couple of pages ago. 

So from what I gather it’s (Risperdal) a very strong D2 blocker, among many others for dopamine and serotonin. Sertonin According to Wikipedia it’s actuallt more potent at 5T2A (0.17 nM) while it’s D2 action is (3.57). 

So since risperidone is “blocking dopamine” does that in turn make dopamine release more effective or sensitive to marijuana? Heck with the whole auto-receptors and pre/post synaptic receptors it gets confusing.

You're right. It is really confusing. Consider what you pointed out about risperidone's higher affinity for 5HT2A than D2. Antagonism of 5HT2A leads to downstream dopamine release. And with a higher affinity for that receptor than for D2, there theoretically would be more dopamine release than blockade at lower doses. And of course keep in mind that as you said, the pre-synaptic D2 receptors are auto-receptors so antagonism will lead to MORE dopamine release.

In a way, dopamine blockers and modulators can enhance the effects of THC. Cannabis already does this now between THC and CBD. THC binds predominantly to the CB1 receptors which are concentrated mostly in the brain. This leads to dopamine release. CBD on the other hand binds predominantly to CB2 receptors which are found pretty much everywhere else in the body but are strongly focused on the surface of white blood cells. Activation of CB2 receptors reduces inflammation caused by our immune system, which is why CBD can be used in certain inflammatory or auto-immune conditions with great effect.

Now bring in the cannabis entourage effect and you have a party. Not only does CBD bind to CB2 receptors, but it also binds to D2 receptors as a partial agonist like Abilify, Rexulti, and Vraylar. With THC increasing dopamine release through activation of CB1 receptors and CBD modulating that dopamine activity by binding to D2 receptors, you kind of have yourself an atypical antipsychotic don't you?

Pure THC administered via IV caused patients to experience psychotomimetic effects akin to something like drug-induced schizophrenia. However an even 50/50 administration of THC/CBD caused no such effects. Cannabidiol does in fact prevent the psychosis-inducing effects of THC. But there is something else that it does in the process that every stoner would be familiar with: couch lock. Cannabis strains with high THC content and negligible CBD can actually be quite activating, but as you introduce more and more CBD, the strain becomes more sedating. CBD on its own can't cause couch lock, but THC and CBD together can be formidable.

So really when you feel stoned and sluggish because of your AAP, just think of it as couch lock, the feeling you get when your synapses are flooded with dopamine and the door on the far side of the synapse is locked! :wtf:

6 hours ago, JJ17 said:

Wikipedia states:

“”Risperidone has more pronounced serotonin antagonism than dopamine antagonism”  which is interesting. I guess I’m just confused as to why being a sertonin blocker at multiple other areas (some very potent some less) would benefit OCD? As from what I understand they in general “reduce dopamine activity” or “stabilize it” or what not, as I know by blocking it can actually caused enhanced _____ and so fourth. Very Complex. But still in general wouldn’t something like haloperidol (which seems to be mainly a potent dopamine blocker) be more effective in treating anxiety and OCD compared to risperidone? Since Risperidone claims that be being a Dopamine antagonist (primarily D2) it leads to “reduced dopamine activity/signaling” which is how the medication works - primarily. But since it also blocks multiple sertonin areas it technically reduces sertonin activity. 

While SSRIS “increase activity” (post wise I believe) or whatever the proper wording is. Point being is it seems to me like risperidone is almost doing the opposite of what SSRIS are suppose to do, no? If so wouldn’t that be counter-productive for OCD/anxiety by blocking sertonin when taking risperidone? It seems that haloperidol is not only a much weaker sertonin blocker, but also seems to hit less sertonin areas? So I wonder if that’s true if meds like haloperidol may be better to combine with an SSRI then Risperidone? Since haloperidol doesn’t block nearly as much sertonin as risperidone? 

Maybe someone here knows  

Risperidone on its own certainly would reduce serotonin activity. However, when you mix it with an SSRI, it kind of does the opposite. Remember that many of those serotonin receptors pre-synaptically are auto-receptors. This means that blockade leads to serotonin release. If you mix this with an SSRI, inhibiting the transporter would perpetuate risperidone's activity and vice versa. Risperidone sees to it that more serotonin is released into the synapse and the SSRI makes sure that it stays there.

An SSRI on its own does slowly over time increase serotonin in the synapse, but this leads to a lot of activation of receptors that possibly shouldn't be activated like 5HT2A. Activation of some of these receptors slows down serotonin release, like an automatic shut-off valve when flow is too high. Risperidone makes sure a dysfunctional shut-off valve doesn't shut off serotonin outflow prematurely and ensures stability between the serotonin and dopamine systems.

Increasing serotonin and not blocking any of the serotonin receptors would lead to inhibition of dopamine release. This is where the SSRI startup effects like insomnia come from. An out-of-balance system where serotonin is high and dopamine is low. Dopamine is supposed to be the calming chemical that provides reward and positive reinforcement to the things that we do. With SSRIs, anhedonia (or loss of ability to feel pleasure) is a hard symptom to crack because it's the one thing that doesn't seem to get better (exception being Wellbutrin/bupropion) unless you add an AAP, which will rebalance the serotonin and dopamine systems after an SSRI has been introduced.

3 hours ago, HydroCat said:

@JJ17

I'm no expert but I have been looking into this technical meds stuff out of interest.

Some points to take into account:

* Not all serotonin receptors are "good". 5HT2C for example inhibits dopamine and noradrenaline release, so being a serotonin 5HT2C antagonist like Risperdal is, may be a good thing.
(Actually, it is an inverse agonist on this receptor, which can be oversimplified as "more antagonist than antagonist")
This is also the reason that Prozac is different from other SSRIs, being a 5HT2C antagonist, increasing N/D activity.

* Blocking of 5HT7 reduces anxiety (again, Risperdal is an Inverse agonist on this one too)

* Some receptors are also present on the same firing neuron and function as auto-receptors that are sort of a "braking" system, so antagonising dopamine D2 auto-receptors can increase neurotransmitter activity by releasing more dopamine (Risperdal, again).

* Serotonin 5HT2A has properties that contribute to psychosis.

Highlighting on 5HT2A and psychosis, one of our most potent hallucinogens is LSD being a super high affinity 5HT2A agonist with a long-acting binding constant.

Some receptors are tricky ones though. While 5HT2C does lead to norepinephrine and dopamine release when blocked and thus antidepressant effect, blocking it also makes you feel hungry. That particular receptor is connected to satiety.

5HT7 is one of the new favorite receptors to antagonize because it can improve SSRI-induced sexual dysfunction. It can also eliminate insomnia by correcting the circadian rhythm. By correcting the sleep cycle, it lends to antidepressant effect.

@HydroCat to understand an inverse agonist, just think of it on a number scale of 0-100. An antagonist has no intrinsic activity at a receptor and thus its number would be 0. A partial agonist at D2 like Rexulti would be a 45. Abilify would be a 60. An inverse agonist is essentially "below 0".

Said another way an agonist pushes a mechanism forward, whereas an inverse agonist is like a hypothetical "vacuum". Antagonizing a receptor has a certain effect. An inverse agonist would just have an even more strong of a downstream effect than an antagonist. In the case of 5HT2C for risperidone, it does truly just mean even more norepinephrine and dopamine release downstream than would be rendered by simply blocking the receptor. It's like the receptor essentially works "in reverse".

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Well, if we are into the discussion :)

Receptors produce a signal when an agonist binds to them, but they also have some signalling activity in absence of such agonist.

An antagonist keeps the receptor in its inactive state, but still allows its basic non-activated low signalling to continue.

Inverse agonist causes the receptor to stop signalling altogether, or at least - less than its normal baseline activity.

It is not entirely different than what you said, just wanted to make clear that the receptor don't reverse its activity but is rather "further blocked" by inverse agonists.

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I’m too high to read all this right now but.... 

 

I think my dopamine must be skyyy high as my “reward system” seems to be in over-drive. This is only in about a bigger half of a gummy or maybe 7.5mg thc. Wowz. I am in Colorado so they make the content well know at stores. 

Because winning a video-game I play daily feels SO REWARDING. Like I’m the king or something for winning, lol. 

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Browri: Thanks for the info.

I’m confused on:

“With THC increasing dopamine release through activation of CB1 receptors and CBD modulating that dopamine activity by binding to D2 receptors, you kind of have yourself an atypical antipsychotic don't you?” 

I thought that atypical antipsychotics worked by modulating dopamine activity in the opposite way or much differently then THC? 

Also in terms of the SSRIS causing the zombie/emotional blunting due to high sertonin and low dopamine levels - that’s kinda odd. I’ve heard people talk about it and knew it was possible but they don’t do that for me. I could (or can) still feel emotions “too much” even at max dose SSRIS.... I actually would like some emotional blunting but I don’t get any. The one side effect I wish SSRIS would give me, and it doesn’t.... As my attachment problem is emotional based so having a way to blunt it, even if only somewhat, would be very nice....

But in theory then you’re saying that risperidone could make it worse (at least for me) as I still have basically all the low sertonin symptoms even being on an SSRI and risperidone...Huh. 

 

But update wise:

Been on it a few weeks now still at 1mg and it doesn’t feel like I’m taking anything.... but then again I’m not sure. As things like THC and nicotine seemed to be more potent: so is it from the SSRI or risperidone? Or both? Guess I won’t ever really know since I increased Zoloft around the same time as starting risperidone, so it could be from upping the Zoloft by 50mg and finally achieving   Therapeutic levels - or it could be from starting the 1mg risperidone. Damn I should have asked my doctor if I could have spaced them out to see which med is doing what (or anything). 

I got ULTRA stressed a couple weeks ago when I decided to hangout with the person I have an attachment on. So I bought cigarettes and beer, and started to smoke again. I quit cold turkey a year or so ago, and have gone on and off many cold turkey in the past 10 years and never having any WD, it honestly felt like nicotine/cigarettes did nothing mentally to me during those 10+ years on and off - the only addictive part that kept me smoking was blowing out smoke and “looking cool”. 

But now after being on SSRI long term and at high dose - or being on Risperidone - or maybe Combo of both - whatever the case  they seem to also intensify nicotine. As I feel that “nicotine buzz”. I also felt slightly better mentally - like more confident. I never got those positive mood boosts from nicotine before.... So I wonder if Zoloft and/or Risperidone is causing the nicotine to release more dopamine and serotonin? Or possibly other things? Or maybe nicotine never did anything mentally before as there wasn’t “much dopamine or serotonin to work with” in the first place - and the SSRI changed that by reuptaking sertonin, and Risperidone by... Well, not sure I figured by blocking dopamine such as D2 it would weak nicotine’s effects

But I haven’t fully read the comments above yet so maybe I should =P 

 

Edited by JJ17

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