Mental Health Coming off Invega (Paliperidone, Xeplion) injections v. 7.0

[Rulomaner]

The opposite happens. If you stop taking an antipsychotic you have inverse tolerance to the antagonism you had for such a long time and so it will be oversensitive.
Infact there are people who take haloperidol for like 2 weeks, stop taking it and they feel energized for a few days more than before taking it. It is a personal experience too.

I don't know specifically every of those cases. Maybe they were taking too much abilify (maybe the dosage that was required to treat an acute psychotic episode and not the maintenance dose) or too little lisdexamphetamine. In any case If you decide to go down this road, I have told you which antipsychotics are the most suitable.

Have you taken any aps or experienced with them?

 

[MephedroneCandy]

Have you taken any aps or experienced with them?

I tried haloperidol, risperidone and aripiprazole.

 

[Mucky]

Ive been 4 months off abilify shots. No erections during the day. No sensitivity (thats by far the worst) I would prefer not having erections but having sensitivity than having erection when I need to but not feeling anything. Sperm is shitty. Just a few drops and if not wattery semen. This is hell mate I am sorry to tell you!
I used to practice sex everyday, and I have experience practising it in this condition. Is hell mate

I’m sorry to that mate , hopefully you will recover sooner rather than later , do you have any other symptoms or is it just sexual dysfunction ? Do you have anhedonia at all ?

 

[Rulomaner]

I tried haloperidol, risperidone and aripiprazole.

And now how do you feel towards them? Do you have any lastimg symptoms or are u on them?

I’m sorry to that mate , hopefully you will recover sooner rather than later , do you have any other symptoms or is it just sexual dysfunction ? Do you have anhedonia at all ?

I have anhedonia, inner restless, no capacity like before to talk, think, process, insomia, no apetit, no libido, no motivation to do anything because I donde feel high from it, I would say the best way to describe it is I cant feel high on life! Nor with other people or alone, its the same shit over and over. Wbu bro?

 

[Kaatrina]

Thank you for replying! I was hoping I didn’t say anything wrong but did you think I actually did a good job, or should I have said things differently?

No, I was glad that you were there to talk to him.

If you started antipsychotics for schizophrenia and they work, do not stop them because of cognitive deficits. An hypodopaminergic tone in most regions in the brain except the striatum which is hyperdopaminergic is normal for schizophrenia and it is responsible for the negative symptoms and partially for hallucinations. Invega exacerbates this hypodopaminergic state in favor of rebalancing striatum.
Abilify fixes it by being a partial agonist instead of antagonist, so you can try switching to it. Cognitive deficits should get better than invega, or even better than baseline. If you still want improvement you can very carefully add lisdexamphetamine to the treatment ALWAYS when you are already stable on antipsychotics. With lisdexamphetamine you can rebalance all hypodopaminergic regions and so treat all the negative symptoms of schizophrenia, while still having protection from positive symptoms by antipsychotics.

The lack of treatment for negative symptoms contributes to the reason of why some schizophrenics do still have positive symptoms when on antipsychotics. For example because the hypodopaminergic tone is associated to hearing problems, it goes in synergy with positive symptoms since the brain is forced to predict a lot aka hallucinate to understand the confused stuff it hears. but psychiatrists don't even know if they're alive, so this isn't being addressed as it should be.

Whatever you choose, I don't think just don't taking nothing is a good solution for a schizophrenic patient because there is good potential of a extremely high quality of life thanks to the right treatment.

Some source if the logical explaination isn't enough: https://www.nature.com/articles/npp2013111

I would love to see a citation on your claims of rebalancing stratum.
I'd love to see a citation on your claim that abilify improves cognitive deficits over baseline.
There is no evidence in your study that shows that lisdexamphetamine "rebalances all hypodopaminergenic regions".

None of those three claims are supported by your study. Your study took 88 very stable people that were already on AP, gave them ADHD med (psychostimulant) for 10 weeks (unblinded!) And then observed them for one week and withdrew them blindly for 3 weeks. Almost half of the participants withdrew from the study in the blinded phase. The study then claims that because people that STAYED ON amphetamine during withdrawal phase had better NSS than those who WITHDREW on placebo during withdrawal phase, it may mean that lisdexamphetamine improves NSS because placebo patients were doing more poorly than those still taking lisdexamphetamine. In my untrained opinion it may also mean that those receiving placebo after being on amphetamine for 10 weeks experienced some withdrawal, but the study does not account for this.

The study authors say "Confirmation of these results with larger, double-blind, and placebo-controlled trials is needed" and "Similarly, expectation bias/placebo effects by participants may have contributed to observed treatment effects during the open-label phase.". This is a pilot trial meant to lead up to a bigger trial in which conclusions can actually be made. This study was done 10 years ago, but we have no further evidence of psychostimulants helping with negative symptoms further.

I would be careful with making such broad sweeping statements off of a study such as this.

Some on this forum along with myself were misdiagnosed with schizophrenia after unspecified psychosis.according to my psych, invega "worked" , and i shouldnt cease it. Like you, my psych and family believed that the effect of the medication caused my "NSS" and that my idea that my "NSS" came from the drug was a positive symptom of schizophrenia. I have lived happily for over three years with no negative or positive symptoms of schizophrenia and no medication. I experienced two subsequent short-term psychoses in that period that could be ascribed to the supersensitivity you describe, or to environmental factors or a non schizophrenic factor.

i think the propensity to diagnose schizophrenia outside the DSMV in the industry and also the common fact that all of us in this forum are here because we are experiencing extreme negative symptoms the we DIDNT experience before the medication should all be considered. You should also consider that our members constantly try and report on the effects of every type of stimulant on the effects we experience (anhedonia among others) and they have no effect.

Lisdexamphetamine? How? Abilify is partial agonist, yes, but theres a trick there. Partial agonist on PREsynaptic and antagonist on POSTsynaptic, which means you are not going to get any fucking dopamine. Why te fuck would you antagonize the post and agonize the pre, it should be the other way round for fuck shake I cant believe this scientists are so stupid!

They say it's because it has a different release system than other ADHD med but can't say why. All authors of the study are employed by shire among other pharmaceutical companies. For once I agree with you. Lmao

 

[MephedroneCandy]

And now how do you feel towards them? Do you have any lastimg symptoms or are u on them?


I have anhedonia, inner restless, no capacity like before to talk, think, process, insomia, no apetit, no libido, no motivation to do anything because I donde feel high from it, I would say the best way to describe it is I cant feel high on life! Nor with other people or alone, its the same shit over and over. Wbu bro?

I was feeling fatigued and without mental acuity on them and my adhd was the same maybe worse. So since I had prescribed them because adhd was missdiagnosed as a strange bipolar disorder not well defined I stopped taking them and now I feel like I never took them. But maybe stimulants reversed the neuroplastic changes that they might did that would give me long term effects. But that is just speculation.

 

[MephedroneCandy]

No, I was glad that you were there to talk to him.

I would love to see a citation on your claims of rebalancing stratum.
I'd love to see a citation on your claim that abilify improves cognitive deficits over baseline.
There is no evidence in your study that shows that lisdexamphetamine "rebalances all hypodopaminergenic regions".

None of those three claims are supported by your study. Your study took 88 very stable people that were already on AP, gave them ADHD med (psychostimulant) for 10 weeks (unblinded!) And then observed them for one week and withdrew them blindly for 3 weeks. Almost half of the participants withdrew from the study in the blinded phase. The study then claims that because people that STAYED ON amphetamine during withdrawal phase had better NSS than those who WITHDREW on placebo during withdrawal phase, it may mean that lisdexamphetamine improves NSS because placebo patients were doing more poorly than those still taking lisdexamphetamine. In my untrained opinion it may also mean that those receiving placebo after being on amphetamine for 10 weeks experienced some withdrawal, but the study does not account for this.

The study authors say "Confirmation of these results with larger, double-blind, and placebo-controlled trials is needed" and "Similarly, expectation bias/placebo effects by participants may have contributed to observed treatment effects during the open-label phase.". This is a pilot trial meant to lead up to a bigger trial in which conclusions can actually be made. This study was done 10 years ago, but we have no further evidence of psychostimulants helping with negative symptoms further.

I would be careful with making such broad sweeping statements off of a study such as this.

Some on this forum along with myself were misdiagnosed with schizophrenia after unspecified psychosis.according to my psych, invega "worked" , and i shouldnt cease it. Like you, my psych and family believed that the effect of the medication caused my "NSS" and that my idea that my "NSS" came from the drug was a positive symptom of schizophrenia. I have lived happily for over three years with no negative or positive symptoms of schizophrenia and no medication. I experienced two subsequent short-term psychoses in that period that could be ascribed to the supersensitivity you describe, or to environmental factors or a non schizophrenic factor.

i think the propensity to diagnose schizophrenia outside the DSMV in the industry and also the common fact that all of us in this forum are here because we are experiencing extreme negative symptoms the we DIDNT experience before the medication should all be considered. You should also consider that our members constantly try and report on the effects of every type of stimulant on the effects we experience (anhedonia among others) and they have no effect.


They say it's because it has a different release system than other ADHD med but can't say why. All authors of the study are employed by shire among other pharmaceutical companies. For once I agree with you. Lmao

Lisdexamphetamine rebalance hypodopaminergic regions because it is just its mechanism of action. It is a noradrenaline and dopamine releaser agent aka NDRA. It is not true there is only a study about it. Even if it was true, it is an high quality study in humans, published on Nature, so it is enough. But here is a metastudy of other similar studies: https://www.sciencedirect.com/science/article/abs/pii/S0920996413001655

As I said it is very possible for antipsychotics to worsen negative symptoms because they are not selective for striatum, this is why I recommended combining lisdexamphetamine.
All my discussions are for people with schizophrenia, not for people with misdiagnosed schizophrenia.
If your schizophrenia was not diagnosed under the rigorous defining criteria of the DSM by someone who evidently de facto is not a professionist even if he is de iure, then re-evaluate your therapy including the possibility of stopping antipsychotics! I took it for granted of course.

If you stopped antipsychotics and you are experiencing long-term effects then you can sue the doctor for medical malpractice but I'm not an expert in the legal field, or you can burn down his house for revenge. In short, do what you want, this is beyond my competence at the moment. And you can take lisdexamphetamine alone to counteract those neuroplastic changes.

 

[Kaatrina]

I was feeling fatigued and without mental acuity on them and my adhd was the same maybe worse. So since I had prescribed them because adhd was missdiagnosed as a strange bipolar disorder not well defined I stopped taking them and now I feel like I never took them. But maybe stimulants reversed the neuroplastic changes that they might did that would give me long term effects. But that is just speculation.

Yeah dude. You totally rebalanced your striatum.

Lisdexamphetamine rebalance hypodopaminergic regions because it is just its mechanism of action. It is a noradrenaline and dopamine releaser agent aka NDRA. It is not true there is only a study about it. Even if it was true, it is an high quality study in humans, published on Nature, so it is enough. But here is a metastudy of other similar studies: https://www.sciencedirect.com/science/article/abs/pii/S0920996413001655

As I said it is very possible for antipsychotics to worsen negative symptoms because they are not selective for striatum, this is why I recommended combining lisdexamphetamine.
All my discussions are for people with schizophrenia, not for people with misdiagnosed schizophrenia.
If your schizophrenia was not diagnosed under the rigorous defining criteria of the DSM by someone who evidently de facto is not a professionist even if he is de iure, then re-evaluate your therapy including the possibility of stopping antipsychotics! I took it for granted of cocourse.

Can you please offer your citations for those three claims that I asked for.

Methamphetamine is an NDRA too. We have plenty of evidence of how it conteracts "NSS" related to invega here on BL. Lmao!

Thanks for that overview. I especially enjoyed the part where they used "data presented at meetings" for their analysis. Did you read the conclusion? This is the conclusion: "Large, controlled clinical trials to further characterize effects of psychostimulants on NSS in carefully selected patients are warranted." This is the same conclusion as your other study. It doesn't support any claims you're making about lisdexamphetamine.

Pertinent:
"Shire Development LLC provided funding to SCI Scientific Communications & Information (SCI) for support in writing and editing this manuscript." Can you find a study that amohetamines should be used to combat NSS that isn't funded by companies that market and sell amphetamines?

Also pertinent:
"Several areas of inadequate study and limitations are identified including small study samples, single-site trials, varying rigor of bias control, the dose and the duration of adjunctive psychostimulant administration, and the potential for development of tolerance."

Your study wasn't "quality" because an unblind study is open to bias.

Many of us didn't experience "worsening of NSS", we experienced "NSS" that was drug-incuced and non-existent before medication introduction
You may be very surprised at how common that type of diagnosis is. Even when not officially diagnosed we are told to stay on APs for years "to be safe"

 

[MephedroneCandy]

Yeah dude. You totally rebalanced your striatum.

Can you please offer your citations for those three claims that I asked for.

Methamphetamine is an NDRA too. We have plenty of evidence of how it conteracts "NSS" related to invega here on BL. Lmao!

Thanks for that overview. I especially enjoyed the part where they used "data presented at meetings" for their analysis. Did you read the conclusion? This is the conclusion: "Large, controlled clinical trials to further characterize effects of psychostimulants on NSS in carefully selected patients are warranted." This is the same conclusion as your other study. It doesn't support any claims you're making about lisdexamphetamine.

Pertinent:
"Shire Development LLC provided funding to SCI Scientific Communications & Information (SCI) for support in writing and editing this manuscript." Can you find a study that amohetamines should be used to combat NSS that isn't funded by companies that market and sell amphetamines?

Also pertinent:
"Several areas of inadequate study and limitations are identified including small study samples, single-site trials, varying rigor of bias control, the dose and the duration of adjunctive psychostimulant administration, and the potential for development of tolerance."

Your study wasn't "quality" because an unblind study is open to bias.

Many of us didn't experience "worsening of NSS", we experienced "NSS" that was drug-incuced and non-existent before medication introduction
You may be very surprised at how common that type of diagnosis is. Even when not officially diagnosed we are told to stay on APs for years "to be safe"

Infact dextromethamphetamine is just a more potent and short acting substance similar to lisdexamphetamine (did you noticed their name contains this very cute and pretty word "amphetamine"?) and it counteracts negative symtomps for sure; this is why a lot of schizophrenic use it. But if someone is schizophrenic this means it potentiates positive symtomps, because as I said the striatum is hyperdopaminergic. This is why you must stabilize the positive symtomps before taking any stimulant.
I will not send you citations for something simple and well understood such as that amphetamines increases dopamine concentration. The citation is the category they are in: "noradrenaline-dopamine releasing agent". And they increase dopamine in all brain regions, including hypodopaminergic ones. About clinical studies, I sent you a metastudy other than the first study. Regarding abilify, I didn't say it solves negative symptoms. Its pharmacological profiles makes it ameliorates them in very severe schizophrenia thanks to its partial agonism. In normal cases, it is just better than typical antipsychotics in not inducing them too much.

If you was missdiagnosed as someone needing APs even if you didn't, like it happened to me, then it is another problem that I dealt in the last paragraph of my last post. As I said psychiatrists don't even know if they are alive.

 

[Kaatrina]

Infact dextromethamphetamine is just a more potent and short acting substance similar to lisdexamphetamine (did you noticed their name contains this very cute and pretty word "amphetamine"?) and it counteracts negative symtomps for sure; this is why a lot of schizophrenic use it. But if someone is schizophrenic this means it potentiates positive symtomps, because as I said the striatum is hyperdopaminergic. This is why you must stabilize the positive symtomps before taking any stimulant.
I will not send you citations for something simple and well understood such as that amphetamines increases dopamine concentration. The citation is the category they are in: "noradrenaline-dopamine releasing agent". And they increase dopamine in all brain regions, including hypodopaminergic ones. About clinical studies, I sent you a metastudy other than the first study. Regarding abilify, I didn't say it solves negative symptoms. Its pharmacological profiles makes it ameliorates them in very severe schizophrenia thanks to its partial agonism. In normal cases, it is just better than typical antipsychotics in not inducing them too much.

If you was missdiagnosed as someone needing APs even if you didn't, like it happened to me, then it is another problem that I dealt in the last paragraph of my last post. As I said psychiatrists don't even know if they are alive.

I didn't ask for a citation on whether amphetamines increase dopamine. I asked for citation on these three claims that are far from simple:
1."An hypodopaminergic tone in most regions in the brain except the striatum which is hyperdopaminergic is normal for schizophrenia and it is responsible for the negative symptoms and partially for hallucinations. Invega exacerbates this hypodopaminergic state in favor of rebalancing striatum."

2."Abilify fixes it by being a partial agonist instead of antagonist, so you can try switching to it. Cognitive deficits should get better than invega, or even better than baseline. " (this is not a claim of amelioration)

3. "If you still want improvement you can very carefully add lisdexamphetamine to the treatment ALWAYS when you are already stable on antipsychotics. With lisdexamphetamine you can rebalance all hypodopaminergic regions and so treat all the negative symptoms of schizophrenia".

You said lisdexamphetamine works when other ADHD meds don't because of its status as an NDRA. I was merely pointing out that many other drugs are also NDRAs but fail to "rebalance the striatum:, when under the effects of invega and so further explanation is needed.

You should expect pushback and to be asked for proof when coming in with large claims of high quality life available on invega through use of stimulant in this forum

 

[MephedroneCandy]

I didn't ask for a citation on whether amphetamines increase dopamine. I asked for citation on these three claims that are far from simple:
1."An hypodopaminergic tone in most regions in the brain except the striatum which is hyperdopaminergic is normal for schizophrenia and it is responsible for the negative symptoms and partially for hallucinations. Invega exacerbates this hypodopaminergic state in favor of rebalancing striatum."

2."Abilify fixes it by being a partial agonist instead of antagonist, so you can try switching to it. Cognitive deficits should get better than invega, or even better than baseline. " (this is not a claim of amelioration)

3. "If you still want improvement you can very carefully add lisdexamphetamine to the treatment ALWAYS when you are already stable on antipsychotics. With lisdexamphetamine you can rebalance all hypodopaminergic regions and so treat all the negative symptoms of schizophrenia".

You said lisdexamphetamine works when other ADHD meds don't because of its status as an NDRA. I was merely pointing out that many other drugs are also NDRAs but fail to "rebalance the striatum:, when under the effects of invega and so further explanation is needed.

You should expect pushback and to be asked for proof when coming in with large claims of high quality life available on invega through use of stimulant in this forum

1) https://www.clinicaladvisor.com/hom...ion-center/schizophrenia-a-clinical-overview/
2) https://sci-hub.se/10.1055/s-0031-1271688
3) No. I said specifically lisdexamphetamine because it is a good candidate since it has a long duration and less rebound (the comedown would put you in a even more hypodopaminergic tone), but every NDRA or NDRI works. But there are even better stimulants in this aspect too.
And I din't talked about invega specifically, but about antipsychotics in general.
I didn't even know what invega is since in my country there are long-acting risperidone decaonate injections instead of its metabolite.

 

[Kaatrina]

1) https://www.clinicaladvisor.com/hom...ion-center/schizophrenia-a-clinical-overview/
2) https://sci-hub.se/10.1055/s-0031-1271688
3) No. I said specifically lisdexamphetamine because it is a good candidate since it has a long duration and less rebound (the comedown would put you in a even more hypodopaminergic tone), but every NDRA or NDRI works. But there are even better stimulants in this aspect too.
And I din't talked about invega specifically, but about antipsychotics in general.
I didn't even know what invega is since in my country there are long-acting risperidone decaonate injections instead of its metabolite.

1. Your article links to the dopamine *hypothesis* on schizophrenia, which can't be proven, fair enough, but says nothing in relation to "invega exacerbating the hypodopaminergenic state in favor of rebalancing the striatum" all it says is that "efficacy demonstrated through dopamine (D2) receptor antagonism for the typical antipsychotics and the combination of D2 and serotonin (5-hydroxytryptamine [5-HT2]) receptor antagonism for the atypical antipsychotics.20It has been reported that for an antipsychotic to be considered effective, it must exhibit a level of dopamine antagonism of at least 60 to 80% because lower levels of dopamine antagonism generally do not produce observable antipsychotic effects, and in about 60% to 70% of patients, schizophrenia may not be adequately controlled.19." I fail to see how efficacy achieved through a required percentage of dopamine antagonism leads to "rebalance".

2. Your study doesn't even address the question of whether abilify can improve cognitive function above baseline , let alone show it

3. Do you believe that all NDRAS and NDRIs can provide an "extremely high quality of life when used in conjunction with APs, or only lisdexamphetamine? What is your criteria for an acceptable rate of rebound? Dependency?

 

[Robchanna]

Anyone else wanna take a shot and help me understand why I can’t get high. I took 5 shots of Invega and can’t feel the euphoric feeling of weed or alcohol. Do you think this is permanent?

 

[BattlingInvega]

Anyone gain back their spirituality?

 

[bowandsparrow]

Anyone else wanna take a shot and help me understand why I can’t get high. I took 5 shots of Invega and can’t feel the euphoric feeling of weed or alcohol. Do you think this is permanent?

Your dopamine receptors are being blocked by the medication. Others on this thread have reported that it comes back over time, but they feel it weaker than before.

 

[Rulomaner]

Its not just about dopamine for the euphoria. Noradrenaline is also being hardly bocked by every AP

 

[Robchanna]

Its not just about dopamine for the euphoria. Noradrenaline is also being hardly bocked by every AP

Do you think it’s permanent

 

[Kaatrina]

Do you think it’s permanent

No, it will come back but it takes a long time

 

[MephedroneCandy]

1. Your article links to the dopamine *hypothesis* on schizophrenia, which can't be proven, fair enough, but says nothing in relation to "invega exacerbating the hypodopaminergenic state in favor of rebalancing the striatum" all it says is that "efficacy demonstrated through dopamine (D2) receptor antagonism for the typical antipsychotics and the combination of D2 and serotonin (5-hydroxytryptamine [5-HT2]) receptor antagonism for the atypical antipsychotics.20It has been reported that for an antipsychotic to be considered effective, it must exhibit a level of dopamine antagonism of at least 60 to 80% because lower levels of dopamine antagonism generally do not produce observable antipsychotic effects, and in about 60% to 70% of patients, schizophrenia may not be adequately controlled.19." I fail to see how efficacy achieved through a required percentage of dopamine antagonism leads to "rebalance".

2. Your study doesn't even address the question of whether abilify can improve cognitive function above baseline , let alone show it

3. Do you believe that all NDRAS and NDRIs can provide an "extremely high quality of life when used in conjunction with APs, or only lisdexamphetamine? What is your criteria for an acceptable rate of rebound? Dependency?

1) God can't be proven, not a scientific hypothesis. Antagonism counteracts agonism. It is a basic biochemical concept. Medications have a dosage that varies to accommodate different patients. It is not a fixed percentage of antagonism. Also probably those percentages are related to the binding without competivity from dopamine, because the AP is the only ligand in vitrio. So in-vivo it is much less and it is inversely proportional to the dopamine concentration.
Invega goes in systemic circulation so it reaches all brain regions, so it antagonize everything it has affinity for. It is another basic biochemical concept.
2) https://www.thieme-connect.com/prod...?device=mobile&innerWidth=980&offsetWidth=980
3) Do not oversimplify, every substance is a specific case in its own, it is not black and white. I just wrote about a good possible candidate, a bad possible candidate is methylphenidate. It also depends on the patient and his metabolism. My criteria for an acceptable rate of rebound is that it does not annoys the patient. Or never if the stimulant has a long half life. I don't know what dependency has to do with everything we are talking about. Dependence happens only in predisposed individuals which are a minority; for sure it does not happen for example to hypodopaminergic individuals. It is normal they are "dependent" on it, just like someone is on AP.

 

[Robchanna]

No, it will come back but it takes a long time

Did it come back for you