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Many antipsychotics are actually delirants - why on earth are they still used!?

dopamimetic

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Chlorpromazine (Thorazine)
Chlorprothixene (Truxal)
Olanzapine (Zyprexa)
Clozapine (Leponex)
Haloperidol (Haldol, not anticholinergic but irreversibly inactivates sigma receptors and is a dopamine inverse agonist - dysphoria and akathisia hell!)
Risperidone (Risperdal, has no real affinity but nevertheless anticholinergic adverse effects are listed)
Quetiapine (Seroquel)

Even Carbamazepine (Tegretol) appears to be one too!

Also most tricyclic antidepressants are strong ACh antagonists - and because of their sedative nature, they are often mixed with one or even multiple antipsychotics, leading to obvious potentiation!! Paroxetine might have a slight effect on the higher dosages as well (maybe confirmed).

all are more or less potent anticholinergics. As we know from things like diphenhydramine (or scopolamine!) they can and do induce nasty delirium with true aural and optical hallucinations, talking with people who don't exist, paranoia, all the negative as well as positive 'schizophrenic' symptoms and the dopamine blockade adds it's own part to the whole picture and so on ... and this is a reality! The only time I had true, unidentifiable hallucinations was on chlorprothixene (Truxal, I think just 150mg or so, and this was before I've done any real drugs, one or two years later I took up to 400mg of diphenhydramine with no delirant effects!) - seeing and talking with people who weren't there, I remember most of the situations and it has been confirmed by multiple persons - I've always thought of this as a weird coincidence of some mental illness but now it completely makes sense! This is just theorising, but I'd speculate that the dopamine actually has a moderating role[1] and antagonising it too much can even potentiate the delirant properties of anticholinergics!?

[1] (see improved impulse control etc. of ADHD people on moderate dosages of stimulants and indeed the atypical amisulpride, which in lower dosages improves dopamine has a less severe adverse reaction profile and actually helps many people - and mostly causes akathisia and dyskinesia in higher dosages from the obvious anti dopamine activity)

Also neuroleptics in general can lead to a serious condition called neuroleptic malignant syndrome which sounds to me like just the escalation of all this!

I've gone psychotic again on olanzapine some years later, this was a bit different (no hallucinations), but very real confusion and loss of reality etc. I've always thought I must be an exception, these are antipsychotics and all that - and I'd bet everyone who's affected thinks sooner or later like that, because everyone around them implicates that he/she has a serious mental disorder e.g. schizophrenia, but ... in the end, I really, really think the whole theory about dopamine being the origin of psychosis is completely flawed and many of these chronic cases of schizophrenia are indeed house-made and just adverse reactions to these toxic neuroleptics!!

Of course, too much dopamine and/or combined with sleep deprivation etc. leads to stimulant psychosis, this is true. But this is a temporary condition that will pass soon with the aid of sleep and/or some sedatives. In those who it doesn't pass, it's very probably an underlying seizure disorder, e.g. temporal lobe epilepsy and these people should get on an anticonvulsant / over-excitation limiting agent like pregabalin, gabapentin, valproate, tiagabine, GABOB, maybe even memantine or riluzole (because we don't have readily available selective 5-HT2A inverse agonists unfortunately also), hell I've even read some anecdotal reports of DXM (sic!) alleviating psychotic symptoms like hearing voices etc., on Erowid if I'm right, maybe I'll find the link again ... after a few weeks or months, they'll be fine again and able to go back to work. No more akathisia, tardive dyskinesia, no more chronically tortured psychotics ... !?

Pharmacy Times: The Anticholinergic Cognitive Burden
PMC: Managing Anticholinergic Side Effects
Anticholinergic drug-induced delirium in an elderly Alzheimer's dementia patient.

Based on these findings, we determine that Ms. B’s delirium most likely is an anticholinergic syndrome from amitriptyline/diphenhydramine toxicity. We discontinue olanzapine after only 2 doses because of its potential anticholinergic effects. from here: Current Psychiatry - Atypical Antipsychotics for Delirium

There is even the shocking practice to give anticholinergics against dyskinesia induced from neuroleptics who might already have anticholinergic effects on their own!!

I really think it might be just so easy. Unbelievable!
 
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i too get fucking baffled by antipsychotics. not because of their anticholinergic properties actually, but because they're, well... ridiculous.

honestly i don't know the whole story but i can't help but feel that this whole idea of antipsychotics (and the old antidepressants) is just something that they came up in the 50's or so, when people didn't know absolutely nothing about mental illnesses, and they simply ended up sticking around, look how chlorpromazine started being used... seriously all they do is turn you into a fucking zombie. .......... i feel once psychiatry evolves more and we understand the brain better, and this is going to have some ethical implications about mental illness and wtv, they will be obsolete.

seriously holding myself not to go on a long rant about this... but i share this sentiment of yours... may be this thread would get more replies over on the Dark Side or Mental Health? idk

also, haloperidol shows MPTP type dopaminergic toxicity (look at its molecule) and that shit is still prescribed... so much trouble in the world
 
It is true that some psychiatric mediactions have anticholinergic effects, but that effect is weak at normal doses and is usually tolerated. Just like with diphenhydramine.

Use of haloperidol is no longer common, but risperidone, olanzapine, quetiapine, clozapine, are the most effective atypical antipsychotics. Quetiapine is actually the only antipsychotic that can be used in Parkinson's patients. It would be suprising if they were not used -- the fact that they have anticholinergic effects is not a good reason to leave folks untreated. Cholinergic blockade is a common off target effect and is almost unavoidable.
 
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If some people in the schizophrenia spectrum might be grouped into subgroup of running low on acetylcholine activity for whatever reason I think it makes sense that we would especially avoid anticholinergics in this subgroup and could go a step further and say that boosting acetylcholine could prove therapeutic.

https://www.ncbi.nlm.nih.gov/pubmed/17467960 - "Subsequent exposure to the choline uptake enhancer MKC-231 antagonizes phencyclidine-induced behavioral deficits and reduction in septal cholinergic neurons in rats." Yes it is indeed a PCP model of schizophrenia but it does seem to help concerning loss of choline acetyltransferase. MKC-231 is Coluracetam by the way. I wonder what's causing the loss of choline acetyltransferase, maybe this applies to substances outside of PCP? How much of the "chronic administration of PCP causes schizophrenia" thing is loss of acetylcholine anyways? Are there other enough other changes that account for the altered behavior outside of acetylcholine? I'm sure the behavior can't be fixed with dopamine antagonists anyways, and are probably made worse by strong anti-cholinergic effects.

I'm piss poor at chemistry but I'd say if we know the anti-cholinergic effects are bad (for acute delirium or long term M1 blockade related amyloid beta problems) but we can't design an atypical antipsychotic that doesn't have anticholinergic effects, then we could boost acetylcholine proportionally to the anti-cholinergic effects. This could be an add-on therapy for patients using APs that have anti-cholinergic effects that are not wanted.

When you say that haloperidol irreversibly inactivates sigma receptors, is this in the same sense that Risperidone irreversibly antagonizes 5-HT7 but that only lasts until the receptor is recycled? Side note about haloperidol, my grandma was actually given it on hospice for agitation (Yes, in the year 2015, in Washington state) It made her worse. We ended up just going through the benzos we had.

I think the main thing we can take away from this for certain is concerning use of "low-level" anticholinergics - you definitely don't want to give them to somebody who is already running low on acetylcholine, i.e an Alzheimer's patient that's losing choline acetyltransferase and a possible subgroup of schizophrenic spectrum people that are in a similar boat.

On a personal note, since extensive Benadryl abuse at a young age, I'm EXTREMELY sensitive to it's anticholinergic effects. A couple pills is absolutely horrible for my psyche, I already have some HPPD/Visual snow genre symptoms, but they get extremely bad on even a little Benadryl.
 
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Five points:

(1) The anticholinergic effects are usually weak to moderate at the doses typically used, so it isn't a problem for most patients.

(2) What is the alternative you are proposing? To leave patients unmedicated? There are not other options available to treat patients with schizophrenia.

(3) Anticholinergic agents are commonly used to treat extrapyramidal symptoms in schizophrenia patients, so it isn't the case that anticholinergics are contraindicated in schizophrenia

(4) It is difficult to design antipsychotic drugs that don't have some affinity for muscarinic receptors because of SAR overlap. Ligands only have to have moderate affinity for M-receptors to potentially produce some degree of antcholinergic side-effects. It is one thing to try to reduce affinity but it is much more difficult to completely eliminate an interaction.

(5) Haloperidol blocks sigma-1 receptors, so it doesn't really matter if one of its metabolites inactivates sigma-1. Either way, someone taking haloperidol is going to have very little sigma-1 activation. As soon as haloperidol is discontinued, sigma-1 receptors will rebound. Bringing up this issue makes it sound like inactivating sigma-1 has profound implications but that isn't known to be the case.
 
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I guess my alternative is if we think the anti-cholinergic effects are causing problems in a subpopulation then we could think about boosting acetylcholine proportionally to the strength of the anti-cholinergic if we can't design a drug that doesn't have anticholinergic effects, though I wonder what boosting acetylcholine does in people who don't have a deficit or whose mental well-being is not bottle-necking at lack of acetylcholine.

If antagonizing M1 does indeed cause increased amyloidosis then I think this should be accounted for in regards to treating diseases long term (short term anti-cholinergic effects aside), there could be long term effects most specifically regarding the elderly (certainly avoid strong anti-cholinergics and the elderly) or a possible subpopulation of schizophrenics that have similar low-acetylcholine pathology, the aforementioned schizophrenics might be on their way to long term problems/amyloidosis already from low acetylcholine activity (which could be functionally akin to M1 blockade?) or they could already be having short term cognitive symptoms from low acetylcholine.
 
http://www.ncbi.nlm.nih.gov/pubmed/26138495 - "Anticholinergic Activity and Schizophrenia - 2015"

"In this article, we review the downregulation of acetylcholinergic activity in schizophrenia and discuss the similarity and difference between Alzheimer's disease (AD) and schizophrenia in terms of acetylcholine (ACh) and anticholinergic activity (AA); then, we propose the use of cognition-enhancing therapy for schizophrenia. As ACh regulates an inflammatory system, when the cholinergic system is downregulated to a critical level, the inflammatory system is activated. We consider the possibility that AA appears endogenously in AD and accelerates AD pathology.

This hypothesis can also be applied to schizophrenia. In fact, even before the onset of the disorder, in the prodromal phase of schizophrenia, cognitive dysfunction exists, and antibodies against astrocyte muscarinic-1 and muscarinic-2 receptors are present in the serum of patients with the paranoid type of schizophrenia. Then we noted that the prodromal phase in schizophrenia might correspond to the mild stage in AD and the acute phase to moderate stage concerning AA. We also think that we should enhance cognition in schizophrenia even in the prodromal phase because as mentioned above, downregulation of ACh is prominent in schizophrenia even in the prodromal phase."

http://www.ncbi.nlm.nih.gov/pubmed/26108886 - "Potentiation of M1 Muscarinic Receptor Reverses Plasticity Deficits and Negative and Cognitive Symptoms in a Schizophrenia Mouse Model. 2015"

http://www.ncbi.nlm.nih.gov/pubmed/25880220 "Antipsychotic-like effect of the muscarinic acetylcholine receptor agonist BuTAC in non-human primates. 2015"

And there appear to be many more recent studies on acetylcholine and mental illness.

I suppose if there was a subgroup of schizophrenia that had an acetylcholine deficit responsible for some of the symptoms, any amount of anticholinergic activity would be going in the completely opposite direction.
 
I guess my alternative is if we think the anti-cholinergic effects are causing problems in a subpopulation...

Most psychiatrists don't think that anticholinergic side-effects are causing major problems in schizophrenia patients. You are really taking a minor issue and blowing it out of proportion. The big problem associated with atypicals is metabolic disease.
 
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC487008/ - "Managing Anticholinergic Side Effects" - Talks a bit of anticholinergic effects related to delirium in the elderly (which I think because of loss of acetylcholine with age they might be the most predictably vulnerable to CNS AC effects), though the study did not include atypicals, it says-

"Delirium occurred in 30% of participants (N = 20). In bivariate and multivariate analyses, high serum anticholinergic activity was associated with delirium (p = .003, OR = 1.95; p = .006, OR = 2.38, respectively). While this study did not include atypical antipsychotics, the high presence of delirium among patients administered medication with anticholinergic properties indicates that physicians need to be attuned to the possibility of central side effects among patients prescribed atypical antipsychotics."

But if there was a subgroup of schizophrenia that had an acetylcholine deficit (which there appears to be) responsible for some of the symptoms, any amount of anticholinergic activity would be opposite of what is needed. Long-term acetylcholine deficits leading to amyloidosis aside.

I'm not saying any of these anti-psychotics are horribly strong anticholinergics (except maybe clozapine is a bit stronger concerning M1, and in a mouse model of PCP-schizophrenia, M1 potentiation was helpful "http://www.ncbi.nlm.nih.gov/pubmed/26108886"), but for myself I lose my mind with 1 pill of Benadryl anymore. Not sure exactly why I'm so sensitive to it, but there could be a subpopulation of schizophrenics that are sensitive to anticholinergics, but the low level affinity of these anti-psychotics aside, my main point is if their problem is acetylcholine deficits we should be going in the opposite direction of anticholinergics, which is what some recent studies are suggesting.
 
If I don't take Haldol, I cease sleeping right and quickly become psychotic.
 
If I don't take Haldol, I cease sleeping right and quickly become psychotic.

I thought you might find it interesting that the D3 antagonism promotes acetylcholine! Not sure how relevant it is to your benefit but thought I would point it out.
http://www.ncbi.nlm.nih.gov/pubmed/26383990
http://www.ncbi.nlm.nih.gov/pubmed/16697046
http://www.ncbi.nlm.nih.gov/pubmed/3925479

I wonder if the diminished a7 receptors found after haloperidol/risperidone regiments could be accounted for by simple down regulation from increased acetylcholine via D3 antagonism, I suppose you could experience not only typical dopamine rebound but a shortage of acetylcholine upon cessation, part of the acetylcholine could conceivably be from excess D3 activity in withdrawals even.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2084358/

I like Risperidone myself, maybe I should try Haloperidol.

I should also point out that acetylcholine is absolutely essential for sleep even though it was classically thought of us a "wakefulness neurotransmitter", ACh agonists promote REM sleep and antagonists decrease REM.
 
Five points:

(1) The anticholinergic effects are usually weak to moderate at the doses typically used, so it isn't a problem for most patients.

(2) What is the alternative you are proposing? To leave patients unmedicated? There are not other options available to treat patients with schizophrenia.

(3) Anticholinergic agents are commonly used to treat extrapyramidal symptoms in schizophrenia patients, so it isn't the case that anticholinergics are contraindicated in schizophrenia

(4) It is difficult to design antipsychotic drugs that don't have some affinity for muscarinic receptors because of SAR overlap. Ligands only have to have moderate affinity for M-receptors to potentially produce some degree of antcholinergic side-effects. It is one thing to try to reduce affinity but it is much more difficult to completely eliminate an interaction.

(5) Haloperidol blocks sigma-1 receptors, so it doesn't really matter if one of its metabolites inactivates sigma-1. Either way, someone taking haloperidol is going to have very little sigma-1 activation. As soon as haloperidol is discontinued, sigma-1 receptors will rebound. Bringing up this issue makes it sound like inactivating sigma-1 has profound implications but that isn't known to be the case.

I think this sums it up very well and will only add it is well known that the anticholinergic effects of any drug are markedly increased in the elderly as compared to younger patients and is where the most toxicity is seen.
 
http://www.ncbi.nlm.nih.gov/pubmed/18651995 - "Antipsychotic property of a muscarinic receptor agonist in animal models for schizophrenia."

This is interesting and Im all for data showing possible new targets for use in schizophrenia and other mental disease, but going back to dopamimetic's original post, what this study doesnt say is that current antipsychotics are ineffective in at least some models of schizophrenia and how a muscarinic agonist may be more efficacious or better tolerated. It is promising that the drug used, oxotremorine did decrease effects in all the models studied, which haloperidol could not but until there is more evidence, we are stuck with what we have.
 
What about all the people put on this poison for drug enduced psychosis ?
I know its self inflicted, but it seems to be the standard treatment
How long if ever do the receptors take to recover/regenerate ?

This stuff is used way too much and should be a last resort, not an industry standard
And especially not forced on people

We're still living in the dark ages
 
The problem is the stigma that comes with all these diagnoses, who will ever listen to someone who's labelled as schizophrenic, even more when it has been a drug induced psychosis etc ... and even if someone does listen to them, if you are in anticholinergic delirium, things don't make sense any more and you're not able to come up with solid arguments. You'll just get the dosage adjusted or another toxic agent on top of all. With luck, one will eventually oppose the adverse effects of the other and maybe one's able to get himself out of the psychiatry and live as a 'recovered' schizophrenic. Usually they will take the neuroleptics at a low dosage for years, in fear of slipping into psychosis again, and experiencing constant dysphoria, asexuality, obesity, whatever.

Then we have all this flawed theory and practice of giving a bunch of widely used drugs against next to every minor or major mental ailment which is like pouring kerosine into a fire for some, once I thought of it being just a problem of a particular subgroup - genetically or whatever - but the more I read, the more I think, about my own experiences, about people I've saw, met, talked with about etc. and the more scientific evidence becomes available, it seems to be a problem that is much more common and affects the majority of people in psychiatry. The downward spiral is real, once you have the schizophrenia diagnosis, you won't get it away again.

We have serious problems out there, yeah, psychopaths mainly, people with unipolar mania to some extent ... but they won't search therapy, just that they are more often found in the upper classes of society or politics and are doing some harm to others.

I suppose if there was a subgroup of schizophrenia that had an acetylcholine deficit responsible for some of the symptoms, any amount of anticholinergic activity would be going in the completely opposite direction.
Think this is really true and might not just be a problem of a small subgroup, but many people experiencing delusions will be more sensitive to anticholinergics. Would make sense, not?

Just read all these reports, we have this Invega Sustenna guy here, and so on ... I think just with those here on bluelight we could fill books! And this are only the people who are still rational enough to question about their experiences, find the right words despite being halfway in delirium and/or have people around them who care!

If you look at the Ki values for e.g. olanzapine, it's not exactly weak at antagonising the muscarinic acetylcholine receptors.

And we have all this exciting new research & evidence about inflammation (genetically and/or immune-related), glutamatergic / cholinergic / adenosinergic imbalances ... N-acetylcysteine makes a really interesting supplement for treatment resistant schizophrenia(!!). NADPH oxidase might be another target - over e.g. apocynin.

Because apocynin is structurally closely related to homovanillic acid, one of the major dopamine breakdown products, this could well explain why antidopaminergics actually work, by antagonising dopamine auto receptors, more dopamine gets released & metabolised into homovanillic acid, in the end increased oxoloacetate, less oxidative stress, less glutamatergic overexcitation etc.. Some indeed get 'antipsychotic' / anxiety / paranoia alleviating effects from low dosages of psychostimulants, and the opposite when they wear off (rebound).

This could make a nice link to stimulant psychosis - when the dopamine gets depleted (and there's already much stress and oxidation going on from sleep deprivation), this escalates --> voila.

But then we could avoid all the dopamine related adverse effects by using a directly acting medicine!

I think we're really into something with the link of choline disruption and psychosis / schizophrenia. These posted findings about Coluracetam etc. are very very remarkable and we should look further into this for sure. Also sarcosine is somewhat interesting.

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I've lived for around a year and a half in Southern France with a novel project where they tried to help people recovering from mental illnesses, and so countless many have all reported the same. Their problems got worse when they entered psychiatry, nobody cared, there is no time, no empathy, just labelling and medication, adverse effects and stigma. Oh, and they had to finally close this lovely little project at the end of 2014, after years of exhausting fundraising etc. because the authorities said no (okay, and the leaders were estranged, because the funder was only psychologist and the neurologist they acquired was .. well, he was an idiot. Everybody felt the same. He didn't take the time to get to know me personally, but wanted to write me off as a 'drug addict' because I've talked a bit too much with people about medications and such..)

Just six months or so ago I watched a chief psych doc in Germany saying "You have psychosis. This won't go away, it lasts your whole life, you'll have to live with it." And he rushed away, leaving a prescription of olanzapine. This is so crazy!

I don't say we should let them untreated at all. But the current treatment strategy is completely flawed and is certainly hurting more than it helps. It has and does destroy countless lives, so few people who experience 'schizophrenia' or 'psychosis' are ever able to live completely normal, sober, happy again without the constant fear of relapsing, hellish side effects, lasting damage, and all this shit.

If it was just about blocking dopamine, we indeed have some good agents available: Sulpride, amisulpride (Solian), reserpine. The sulprides actually help some psychotics much better than the traditional antipsychotics, they don't worsen psychosis for sure, but still have the akathisia and dyskinesia problems.

--

I've been through all this shit. Look, I know I'm very lucky to be here right now in this sobriety, to be able to think about these things rationally and without hearing voices or seeing pink elephants outside ... or experiencing the hell of akathisia and dysphoria from dopamine blockade, etc. and so on. I've done a shitload of drugs in my life out of curiosity and self-medication attempts, and nothing, really nothing brought me closer to schizophrenia than antipsychotics (together with all the psychiatric 'care'). Repeatedly!! I might be an extreme case, but it is the reality. I just had real luck and somehow my brain recovers very quickly. But if I hadn't managed to get the hell out of psychiatry, I'd be a babbling psychotic moron now. Granted, it's a bit weird to take a cough medicine and one for Alzheimer's daily when I don't have either ailment, but this is backed by solid robust scientific evidence and not just implications and theories that aren't proven but can't be disproven because nobody cares to look straight enough at them with common sense and see the obvious problems. It would certainly feel much more wrong to give potentially delirium inducing medicine to people suffering from delusions. And when I'd gradually discontinue these meds, I wouldn't rush into psychosis either. I'd just be depressed, anxious, maybe a bit paranoid again.. and I've never lost hope, unless under strong dopamine blockade. This is hell on earth.

You absolutely need dopamine to feel alive and happy (and for motor skills too). And I'm not exactly proud to have achieved this state by myself, to be honest, it scares the hell out of me to see the reality so clear and the implications that come with when all say i'm such a weak person mentally, also that I have to be very, very cautious because if I'll ever get into acute psychiatry again, it will continue ... but it's okay, I won't be able to stop at last, I just happen to have this energy and hope in me that's driving me to get up every day again and be happy about the nature and the sun outside.. and that I'm free to do what I want, able to feel all these feelings.. :)

--

Really, as I've said, many people would very probably be much better off with anti-excitatory agents like the anticonvulsants (especially gabapentin, pregabalin, tiagabin, valproate, GABOB, maybe lithium), memantine, riluzole, clonidine, sometimes even dextromethorphan or just straight sedatives - mirtazapine, hydroxyzine, tripelennamine, trazodone, benzodiazepines, whatever.

--

And look at the Soteria project. This is the right way to go!! :)

Soteria is a community service that provides a space for people experiencing mental distress or crisis. Based on a recovery model, common elements of the Soteria approach include primarily non-medical staffing; preserving resident's personal power, social networks, and communal responsibilities; finding meaning in the subjective experience of psychosis by "being with" clients; and no or minimal use of antipsychotic medication (with any medication taken from a position of choice and without coercion).[1]

Soterias were open — they had no restraint facilities for young psychotic patients, mostly at their onset. Loren Mosher, who founded the Soteria experience, showed that treating psychosis also in the acute phase is possible without using restraint methods.[2]

Soteria houses are often seen as gentler alternatives to a psychiatric hospital system perceived as authoritarian, hostile or violent and based on routine use of psychiatric (particularly antipsychotic) drugs. Soteria houses are sometimes used as "early intervention" or "crisis resolution" services.
 
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Generic haldol or name brand (but not generic) Zyprexa are my faves. Antipsychotics are a godsend for (meth)amphetamine induced psychosis. Besides the movement disorders, their main drawback is dramatic (50 pounds for me) weight gain. The weight gain is reversible in a couple o months if you quit taking them, but like I said, I'm kind of dependent on them apparently. Every time I quit it isn't pretty. Not trying to defend them at all. I really wish I could quit taking them.
 
Maybe that old haloperidol indeed isn't the worst thing seeing it's sigma inactivation - sigma1 receptors are suggested to be excitatory and could lead to increased glutamate release. The dopamine inverse agonism could contribute its own to more dopamine release and the said downstream mechanisms. But the side effects are horrible probably and it needs to be dosed very, very carefully because too much sigma antagonism can also cause cell death (have to search the source). And if the MPTP like toxicity neurotic suggested is true, then it's really really bad on the long run. But it could be that it's dosage dependent and just has a very narrow dosage range.. or should be given with a tiny dosage of selegiline / rasagiline to prevent that ... or N-acetylcysteine ...

But there is really no reason for generic olanzapine to be any different than the original brand... you should know that ;)
 
A new client-led therapeutic respite house (based on the Soteria concept) now exists in my little city I'm proud to say. People go there when they are feeling an imminent psychotic crisis looming--they go to be safe and supported and to receive the therapeutic benefits of interactions with peers. I just went to a community meeting which had many speakers that have used it and found it incredibly beneficial not only in shortening the episode but sometimes heading it off altogether, not to mention all the side benefits like self-esteem and feelings of empowerment and hopefulness. Second Story
 
Yeah, this is exactly what we need all over the world, together with some completely new drugs like sigma & kappa antagonists, 5-HT2A inverse agonists and subtype-selective serotonergics in general, more selective glutamate modulators etc ... (not to forget about the real possibility of opioid agonists that lack tolerance development & respiratory depression) !! :)

Why are there so few creative, innovative people at the crucial positions!? We are really good in hindering innovation somewhat.
Hey, I'm just a crazy unconventional-thinking disso nerd. Why do I have to come up with all this stuff!? 8) :? ;)
 
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