22 replies to this topic

[Galaxyshock]

I've been doing some research on schizophrenia and the brain, also using ChatGPT to test the relevance of some of my ideas when it comes to the pathology.

 

NMDA-dysfunction is the core of schizophrenic brain abnormalty. What causes this dysfunction is elevated levels of Kynurenic acid (KYNA), a tryptophan metabolite that is an endogenous NMDA-antagonist. 

• Postmortem studies show increased KYNA in brains of schizophrenia patients.

• CSF measurements reveal higher KYNA levels in living patients.

• Animal studies link raised KYNA with schizophrenia-like behaviors.

• Pharmacological interventions that reduce KYNA (e.g., KAT II inhibitors) are being explored as potential treatments.

The NMDA-antagonism causes the downstream effect of dopamine excess and other neurotransmitter abnormalties.

 

What also supports the NMDA-dysfunction hypothesis:

• NMDA-antagonist dissociative drugs like Ketamine and PCP mimic schizophrenia symptoms more accurately than any other models
• NMDA-agonists treat schizophrenia symptoms
• Clozapine is the superior antipsychotic because it releases glutamate and D-serine, which are endogenous NMDA-agonists

What causes the elevated levels of Kynurenic acid?

• Abnormalities in the kynurenine pathway during brain development (e.g., in utero) might predispose individuals to schizophrenia later.

• Stress, inflammation, or maternal infection can shift tryptophan metabolism toward more KYNA production.

Most often first episode psychosis is triggered by a traumatic event, chronic stress, drug abuse or physical illness. In these situations the person may feel unable to operate in the rational prefrontal thinking-planning-executing manner and is incapacitated which triggers dissociation as a primal mechanism to an overwhelming situation. The neurochemical that makes this dissociation possible is Kynurenic acid.

 

What can be done?

 

"Ways to lower KYNA include direct enzyme inhibition (KAT II inhibitors), pathway rebalancing (KMO activators), reducing inflammation, and lifestyle changes like exercise that divert kynurenine metabolism. Most pharmacological options are still experimental, but lifestyle and anti-inflammatory approaches are practical today."

 

Medications and supplements that target the NMDA-receptors - while they don't lower KYNA levels they treat the malfunction that it causes.

• Clozapine is the heavy artillery in schizophrenia treatment as explained earlier, it is the only known antipsychotic that treats the glutamatergic dysfunction. Unfortunately it has the side effects of atypical antipsychotics because of the antagonism of several different receptors and also the rare neutropenia risk so Clozapine should usually only be used if other medications and therapies fail. Clozapine is also a GABA-B agonist which is anxiolytic and the metabolite norclozapine is delta-opioid agonist which is antidepressive, contributing to its therapeutic effects.
• Sarcosine is a co-agonist of NMDA at the glycine site
• Theanine is a partial co-agonist at NMDA receptors
• D-aspartic acid is NMDA receptor full agonist
• Panax Ginseng seems to have modulatory effects at the NMDA-receptor and in studies decreases flat affect in schizos (most likely through 5-HT2A agonism)
• Bacopa Monnieri modulates NMDA-receptor function and has some evidence base of treating cognitive dysfunction in schizophrenia
• Pregnenolone is a positive allosteric modulator of NMDA-receptors

Kynurenic acid is also antagonist of the nicotinic acetylcholine receptors which causes cognitive deficits. No wonder the majority of schizophrenics self-medicate with Nicotine. The cholinergic system seems to deal with raw information received from surroundings so targeting this pathway can help as seen with the novel antipsychotic muscarinic agonist Cobenfy.

 

This is still quite simplified theory as there are various factors that influence the pathophysiology of schizophrenia and as seen in the Open Dialogue Model schizophrenia can be treated without resorting to antipsychotic medications at all. The key seems to be to deprogram this chronically maladaptive Kynurenic acid/dissociative pathway from the brain and the individual by providing safe environment and more healthy coping mechanisms to stress or other triggers. Current long-term antipsychotic medications as sole treatment most often result in poor life quality because they don't target the core of NMDA-dysfunction and usually also worsen negative symptoms of the disease by blocking dopamine and serotonin receptors in a forceful manner making normal neurotransmitter firing impossible.

 

Feel free to comment or share your ideas concerning this devastating yet fascinating disease. 

[YoungSchizo]

Clozapine is the heavy artillery in schizophrenia treatment as explained earlier, it is the only known antipsychotic that treats the glutamatergic dysfunction. Unfortunately it has the side effects of atypical antipsychotics because of the antagonism of several different receptors and also the rare neutropenia risk so Clozapine should usually only be used if other medications and therapies fail. Clozapine is also a GABA-B agonist which is anxiolytic and the metabolite norclozapine is delta-opioid agonist which is antidepressive, contributing to its therapeutic effects.
Sarcosine is a co-agonist of NMDA at the glycine site
Theanine is a partial co-agonist at NMDA receptors
D-aspartic acid is NMDA receptor full agonist
Panax Ginseng seems to have modulatory effects at the NMDA-receptor and in studies decreases flat affect in schizos (most likely through 5-HT2A agonism)
Bacopa Monnieri modulates NMDA-receptor function and has some evidence base of treating cognitive dysfunction in schizophrenia
Pregnenolone is a positive allosteric modulator of NMDA-receptors
Kynurenic acid is also antagonist of the nicotinic acetylcholine receptors which causes cognitive deficits. No wonder the majority of schizophrenics self-medicate with Nicotine. The cholinergic system seems to deal with raw information received from surroundings so targeting this pathway can help as seen with the novel antipsychotic muscarinic agonist Cobenfy.

 

• Clozapine is quite dangerous for the liver and has quite the hassle with bloodwork being done so frequently so I won't be trying that anytime soon or ever.
• Sarcosine was a life saviour for me, if it wasn't for Sarcosine I would be locked up for life!!!
• Theanine I tried in pill form and drinking tea (lots of it). Never noticed anything like some other do notice it's effects.
• D-Aspartic Acid was really antidepressive for me but I had crashes on it make me more depressed. Cycling helped.
• Bacopa Monnieri I tried as a nootropic but didn't notice anything on it.
• Panax Gingseng I can't say much about it it was always mixed with some other stuff. I don't know for sure but I think my multivitamin has Panax Gingseng in it but I'm not really sure.
• Pregnenolone I tried when was off antipsychotics. I want to say yes it helped but am not sure because I still went psychotic on it. But my body and muscle's were defined quite nicely on it. No way my body can look that muscular and defined when on antipsychotics. Allapregnenolone I'm interested in, but you can only get it as medication for postpartem psychosis.
• Can't go without nicotine. I was a heavy smoker and still am since they killed vaping pretty much in the Netherlands with their fake cancerous news and it helps children to cigarettes news.
• Cobenfy will be on the market in Europe next year second half, can't wait to try it!!

[YoungSchizo]

Feel free to comment or share your ideas concerning this devastating yet fascinating disease. 

 

I ticked well researched yet I also must should give you a thumbs down my @galaxyshock friend!

 

It is among fascinating and there's too little attention for it hence the fact Cobenfy is the FIRST drug in 70(!) YEARS(!) that works differentely than the standard Zombifying drugs which is accepted as a to they have too much dopamine bruh!

 

Them fuckers in psychiatry fucked my whole life since they treat you untreatable!!

Edited by YoungSchizo, 09 September 2025 - 05:31 PM.

[Galaxyshock]

Hey man, thanks for sharing your experiences with the NMDA-agonists. Did you find them help with negative symptoms such as anhedonia?

 

Yeah schizophrenia is still quite poorly understood condition yet pharmaceutical companies have been satisfied with the current antipsychotic medications as treatments because they do work for positive symptoms to some extent. Cobenfy is definitely welcomed change in this trend having completely different mechanism of action but still isn't nowhere near a cure for the disorder.

 

I'm going to start looking into the endocannabinoid system next, I think there's potential discoveries to be made. We know that THC has the highest rate of triggering schizophrenia from drugs of abuse whereas CBD shows opposite effects having antipsychotic properties.

 

Evenamide is another novel antipsychotic agent that works through unique mechanism:

 

"Evenamide works by being a highly selective, state-dependent inhibitor of voltage-gated sodium channels (VGSCs). It targets the inactivated state of the channel, leading to the normalization of glutamate release caused by aberrant neuronal activity without affecting basal glutamate levels or normal neuronal excitability. This unique mechanism is believed to address the underlying glutamatergic dysfunction in conditions like schizophrenia, offering a potential add-on therapy for patients with treatment-resistant schizophrenia (TRS)."

[YoungSchizo]

Hey man, thanks for sharing your experiences with the NMDA-agonists. Did you find them help with negative symptoms such as anhedonia?

 

I'm going to start looking into the endocannabinoid system next, I think there's potential discoveries to be made. We know that THC has the highest rate of triggering schizophrenia from drugs of abuse whereas CBD shows opposite effects having antipsychotic properties.

 

 

 

Only Sarcosine helped with negative symptoms. For me it was like 90% positive symptoms 40% negative and anhedonia and 15% cognitive.

 

CBD is quite interesting when you smoke that good stuff from the UK. 

[Galaxyshock]

Good to hear Sarcosine helps! It certainly is a safe supplement and a good augment to antipsychotic medications.

 

I may have been a bit too straight forward with my original post and some may get the impression that the current antipsychotic medications are a failure. Just because the mentioned NMDA-agonists can effectively treat the glutamatergic dysfunction in theory, they are still not studied long-term as sole therapy for schizophrenia. So people shouldn't quit their antipsychotic medications but consider these NMDA-agonists supplements as augmenting strategies. I do think that something like Cobenfy+Sarcosine or Aripiprazole+Sarcosine could have efficacy closer to Clozapine in treating the disorder than an AP med alone and perhaps the dose of the medication can be reduced a bit. But tread carefully regardless. 

 

The Kynurenic acid reducing therapies will most likely be the next big thing when it comes to solving Schizophrenia, at least everything seems to point towards that. But the compounds that target KYNA are still experimental and perhaps simply blocking KYNA production isn't exactly the solution. I mean this neurochemical isn't there to just do harm, it plays its role in "normal" individuals but chronically elevated it seems to lead to maladaptive neurotransmitter imbalances.

 

@YoungSchizo does schizophrenia.com forums work for you? I tried to sign up there but it says registering is blocked from my IP address for some reason. I would have posted my research there too as I'm sure people would find it interesting. 

[YoungSchizo]

Good to hear Sarcosine helps! It certainly is a safe supplement and a good augment to antipsychotic medications.

I may have been a bit too straight forward with my original post and some may get the impression that the current antipsychotic medications are a failure. Just because the mentioned NMDA-agonists can effectively treat the glutamatergic dysfunction in theory, they are still not studied long-term as sole therapy for schizophrenia. So people shouldn't quit their antipsychotic medications but consider these NMDA-agonists supplements as augmenting strategies. I do think that something like Cobenfy+Sarcosine or Aripiprazole+Sarcosine could have efficacy closer to Clozapine in treating the disorder than an AP med alone and perhaps the dose of the medication can be reduced a bit. But tread carefully regardless.

The Kynurenic acid reducing therapies will most likely be the next big thing when it comes to solving Schizophrenia, at least everything seems to point towards that. But the compounds that target KYNA are still experimental and perhaps simply blocking KYNA production isn't exactly the solution. I mean this neurochemical isn't there to just do harm, it plays its role in "normal" individuals but chronically elevated it seems to lead to maladaptive neurotransmitter imbalances.

@YoungSchizo does schizophrenia.com forums work for you? I tried to sign up there but it says registering is blocked from my IP address for some reason. I would have posted my research there too as I'm sure people would find it interesting.

When you post on the forum of schizophrenia.com make sure to make the 'take alongside antipsychotics warning'. The moderators there are wankers, if you don't post the warning they may delete your post. I also doubt that it makes much difference if you post your theory there. There are only a few smart minds that think out of the box and actually try your suggestions.

As for the reach, I can reach the forums but the site/forum is fragile. One DDoS attack and the site will be down for months. It is owned by a guy that makes it poorly save for attacks. (From what I remember it is owned by a non schizophrenic brother of a schizophrenic brother whom committed suicide). The site itself is also poorly maintained about the latest news and innovations.

Edited by YoungSchizo, 12 September 2025 - 07:51 AM.

[YoungSchizo]

 

 

Evenamide is another novel antipsychotic agent that works through unique mechanism:

 

"Evenamide works by being a highly selective, state-dependent inhibitor of voltage-gated sodium channels (VGSCs). It targets the inactivated state of the channel, leading to the normalization of glutamate release caused by aberrant neuronal activity without affecting basal glutamate levels or normal neuronal excitability. This unique mechanism is believed to address the underlying glutamatergic dysfunction in conditions like schizophrenia, offering a potential add-on therapy for patients with treatment-resistant schizophrenia (TRS)."

 

What else can you tell about Evenamide. From the little research I done it's still not available in the USA. Phase III studies started in 2021 in Europe but I can't find it in the future list of schizophrenia medication to be approved by the EMA or not. KARXT (Cobenfy) is sheduled for next year.

 

There was also a nootropic in the pipeline, let me look that up, Iclepertin. I see phase III has not reached statistical signifance over placebo and they disconued it.

 

The thing with schizophrenia drugs is that it always fails in phase III. This has been a major issue. Either the enrollment is not right or either some may benefit big time with it but the label schizophrenia is put on everything, that, in the end, in the past 20 years nothing passes through phase III

[Galaxyshock]

Alright yeah I'll see if I can sign up through VPN or something as it is blocking my own IP from the site for some reason. Good point, I'm no psychiatrist but just a neuroscience geek, so my advice aren't replacement for a doctor's prescriptions hehe. 

 

I haven't looked more into Evenamide but there have been other sodium channel blockers around already, not sure about their antipsychotic potential though. Kava is a herbal sodium channel blocker, perhaps this mechanism is relevant in Kava's ability quiet the mind. I wouldn't be surprised if Kava showed efficacy for psychotic anxiety and its sociability improving effects could perhaps treat the asocial tendencies on schizophrenics. 

 

Nefiracetam is perhaps the best compound from the racetam family for schizos:

 

"Nefiracetam's primary mechanism involves facilitating hippocampal synaptic transmission by activating presynaptic nicotinic acetylcholine (ACh) receptors and L-type calcium channels, which boosts the release of neurotransmitters like acetylcholine and GABA. It also interacts with NMDA receptors, acting as a co-agonist, and influences protein kinase C (PKC) and cyclic AMP-dependent protein kinase (PKA) pathways. These actions collectively improve memory and cognition by enhancing cholinergic, GABAergic, and monoaminergic systems."

[YoungSchizo]

 

"Nefiracetam's primary mechanism involves facilitating hippocampal synaptic transmission by activating presynaptic nicotinic acetylcholine (ACh) receptors and L-type calcium channels, which boosts the release of neurotransmitters like acetylcholine and GABA. It also interacts with NMDA receptors, acting as a co-agonist, and influences protein kinase C (PKC) and cyclic AMP-dependent protein kinase (PKA) pathways. These actions collectively improve memory and cognition by enhancing cholinergic, GABAergic, and monoaminergic systems."

 

I tried Nefiracetam it gave me a weird sort of high but without triggering positive symptoms. Are the racetam's still popular, I barely see reports of it. It's not a hype anymore.

[Galaxyshock]

I tried Nefiracetam it gave me a weird sort of high but without triggering positive symptoms. Are the racetam's still popular, I barely see reports of it. It's not a hype anymore.

 

Ok perhaps Nefiracetam doesn't target the neurotransmission in an optimal way. I think the popularity of racetams decreased in 2010s, partially because lack of vendor availability.

 

Disturbances in amino acid metabolism appear to be relevant in schizophrenia. The more I look into this disorder, the more complex it gets. 

 

Beta-alanine supplementation could help:

 

"While beta-alanine isn't a direct treatment for schizophrenia, it is a precursor to L-carnosine, which has shown some promise for improving negative and cognitive symptoms by interacting with N-methyl-D-aspartate (NMDA) receptors. Research suggests a potential link between schizophrenia and altered amino acid metabolism, including beta-alanine and histidine, and studies on L-carnosine have indicated potential therapeutic benefits for schizophrenia, though evidence remains inconclusive."

 

Cognitive and negative symptoms in schizophrenia with L-Carnosine adjuvant therapy – A randomized double-blind placebo-controlled study

https://bpspubs.onli....1002/prp2.1074

 

There is also plenty of evidence suggesting schizophrenia is an inflammatory state and current antipsychotics don't work for that, sometimes even making it worse. Nickname Hip once mentioned N-acetyl-glucosamine works to dampen neuroinflammation, not sure if it works on schizo brain though.

Edited by Galaxyshock, 15 September 2025 - 12:55 AM.

[YoungSchizo]

Ok perhaps Nefiracetam doesn't target the neurotransmission in an optimal way. I think the popularity of racetams decreased in 2010s, partially because lack of vendor availability.

 

Disturbances in amino acid metabolism appear to be relevant in schizophrenia. The more I look into this disorder, the more complex it gets. 

 

Beta-alanine supplementation could help:

 

 

 

Cognitive and negative symptoms in schizophrenia with L-Carnosine adjuvant therapy – A randomized double-blind placebo-controlled study

https://bpspubs.onli....1002/prp2.1074

 

There is also plenty of evidence suggesting schizophrenia is an inflammatory state and current antipsychotics don't work for that, sometimes even making it worse. Nickname Hip once mentioned N-acetyl-glucosamine works to dampen neuroinflammation, not sure if it works on schizo brain though.

 

Beta-alanine I tried and L-Carnosine because they are added to bodybuilding supplements. Never noticed something though.

 

N-acetyl-glusamine I didn't try.

[YoungSchizo]

If someone is interested in this topic and reading this, maybe we/he/she can organize groupbuy for Iclepertin through China or something. GlyT1 inhibitor, seems like it's worth a serious shot even though they failed phase III and disconued persuing to get it on the market.

[Galaxyshock]

If someone is interested in this topic and reading this, maybe we/he/she can organize groupbuy for Iclepertin through China or something. GlyT1 inhibitor, seems like it's worth a serious shot even though they failed phase III and disconued persuing to get it on the market.

 

Do you use Discord? We have nootropics channel there where group buys can also be discussed. I can send you an invite link if you want. 

 

I started digging into the endocannabinoid system a bit. It seems to also lead back to the Kynurenic acid theory.

 

Evidence suggests endocannabinoid system activity can increase KYNA production.

• Experimental studies (rodent and ex vivo brain models) show that activation of CB1 receptors or treatment with anandamide can raise KYNA levels in the brain.

• The mechanism appears to involve astrocytes, which are the primary site of KYNA synthesis. Endocannabinoids acting on CB1 receptors in astrocytes enhance kynurenine aminotransferase activity, which converts kynurenine to KYNA.

• THC, which mimics endocannabinoid activity at CB1, has also been shown to elevate KYNA levels, which might help explain its psychotomimetic effects.

• Conversely, CB1 antagonists (like rimonabant) can reduce KYNA levels.

 

Relevance to Schizophrenia

• Since both elevated KYNA and ECS dysregulation are linked to schizophrenia, this interaction may be a critical mechanistic bridge:

  • Excess endocannabinoid activity → ↑ KYNA → ↓ NMDA and α7nAChR signaling → cognitive dysfunction & psychotic symptoms.

• This fits with the NMDA receptor hypofunction hypothesis of schizophrenia.

[YoungSchizo]

 

Do you use Discord? We have nootropics channel there where group buys can also be discussed. I can send you an invite link if you want. 

 

 

 

 

I have Discord but rarely use it. idk if a invite is neccesary, bet in that channel there's just a few schizophrenics to organize a group-buy.

[Galaxyshock]

I have Discord but rarely use it. idk if a invite is neccesary, bet in that channel there's just a few schizophrenics to organize a group-buy.

 

Alright yeah, might be hard to organize one. I've also been thinking about forming a study group for mental disorders but I'm not sure if people are interested.

 

I'm now starting to look into Sigma-receptors, those are rather unknown area to me but they seem relevant to schizophrenia and other mental disorders. There's also delta glutamate receptors which seem interesting target but another area I'm not well educated in .

 

I preduct within 10 years there will be medications that target the schizophrenia core problems in a way that people with the disorder can live fulfilling lives instead of throwing them into zombified never ending disability. Cobenfy and other medications indicate that there's still interest producing effective pharmaceutical interventions and other treatment plans like the open dialogue model show that better outcomes are possible.

[YoungSchizo]

 

 

I preduct within 10 years there will be medications that target the schizophrenia core problems in a way that people with the disorder can live fulfilling lives instead of throwing them into zombified never ending disability. Cobenfy and other medications indicate that there's still interest producing effective pharmaceutical interventions and other treatment plans like the open dialogue model show that better outcomes are possible.

 

That's also what they said 20 years ago.. Even talking about a cure within 10 years back then.. And I still get shot monthly with a 60's Haldol in my ass in 2025.   

 

I dunno maybe Elon Musk might one day try his mindreading machine on schizophrenics, I really would like see the outcome of that.

 

Last Thursday there was a female PhD from my city who published a paper (whom studied at Harvard before) talking about hallucinations and that everyone hallucinates once in a while but schizophrenics really hallucinate where there own voice/speech come from whitin their own brain (like we didn't know that). And talking BS that females are more vunerable to psychosis (especially during meno-pauze) then men and everyone should get personalized medicine from the current arsenal.. Dumb sexist bitch 

 

I wanted to ask you to dig into a supplement which is made out of mushrooms (I believe) and has caught attention of scientist and the community of schizophrenia.com attention the past years but that damn site doesn't work again.. I'll ask later if I can find it. 

[Galaxyshock]

Yup the psychiatric drug development is rather disappointing, but I try to remain optimistic that there is intention to treat this disorder better than what the current neuroleptic drugs are capable of.

 

I think there's some evidence of schizophrenic brain operating similar to a person that is asleep. I mean we all hallucinate during REM-sleep, it's just that when similar state enters the wake-time consciousness that shit hits the fan. Perhaps increasing histaminergic signaling would also treat psychotic disorders.

 

I can't seem to sign up to schizophrenia.com it still says my IP is banned, oh well...

[YoungSchizo]

 

I think there's some evidence of schizophrenic brain operating similar to a person that is asleep. I mean we all hallucinate during REM-sleep, it's just that when similar state enters the wake-time consciousness that shit hits the fan. Perhaps increasing histaminergic signaling would also treat psychotic disorders.

 

I can't seem to sign up to schizophrenia.com it still says my IP is banned, oh well...

 

That happened to me in my last episode.. I was talking to my mum that I was dreaming and this and that happened.. She thought it was actually a dream.. My spouses and mom and dad eventually knew I was hallucinating.. But them fckers at the psychiatry didn't want me admitted and I ended up hurting myself.. fcktards!     

 

Try via phone to get on their site.. my PC also doesn't allow me on their site.

[bullGenteel]

I haven't read this thread, ha ha. I'll share a bit more about my prior expereinces.
 
(edit: I read the first post now. There are a lot of overlap with what I wrote. I think I read this post last year. Pretty much all I wrote was based off a couple researchers work. There work does remind me of ideas found through out this site. I don't really delve too much into the science. Some of the work of said researchers is older but still relevant I assume. )

I couldn't really add much in the way of understanding the science of neuro transmitters and such. I did have some semi-formed idea seem to strike me today about OCD and psychosis. All my ideas are usually semi-formed due to my imbalanced IQ, moderate brain injury, etc. Also one can keep in mind I think I'd have to complete at least one more round of Questforlife's progentor-reversioning and proliferating protocol ( my slang not his) in order be more sound in functioning. I expect it may help me with some of my intelligence deficits in the long run too. Judge me if you want I come from a humble, blue collar background and I was exposed to nicotine in the womb, which may result in a less developed hypothalamus or what have you. I may or may not have took notes from 2 years ago when I read up on it to the best of my ability at the time, which isn't much better now. It can affect working memory and some emotional regulation so executive function. I suspect Questforlife's protocol may be helpful to fix that area of damage as well as my more severe brain damage from a serious accident. I am also not taking any nootrophics the last 2 weeks or so, and I now feel I can still function moderately well compared two a few months back when I killed off a chunk of sentient like damaged cells that resulted from said accident. I am also in the first 24 hours of a fast, so not too bad for any dampening cognition, as of yet.

[bullGenteel]

A bit more abut my thoughts on mental health. Maybe a little side tracking as it is, so people could skip this post:

I am anonymous on here, usually I would share this with people who I know well. I've shared some stuff like I just mentioned so here goes. I was misdiagnosed with psychosis as an early teen. I believe I have moderate OCD, which does sound to be a common misdiagnosis I have found out. I also have a few personality disorders. I'll share a bit about my thoughts on mental health. I remember skimming thru the mask of sanity 5 years ago. It was kinda boring and unrelated to me with all the low functioning psychopaths, but did mention a doctor colleague that was different but not sounding like me much either. I think I can have more sympathy for traditional socio/political views. I used to think of myself as left leaning, but I feel it's really not conducive to setup one up to potentially do the hard work to be able to thrive or flourish, so I have moved to more progressive conservative considerations, but I digress, perhaps with that future shift in the back of my mind; it prompted wondering why someone from the author's generation would choose to specialize in psychopthy, when the times would deem degenerates, period. I could see it today how people make everyone a victim, even not so upstanding of personage. But the author's premise was he felt bad for the families, he sorta saw psychopathy, perhaps a bit similar to schizophrenia, only in that it pops up almost out of no where from parents who were perfectly normal.

I kinda see the author's views to fall in line with dysgenic theory that I have familiarized myself a bit on. Based on that theory there would likely have been an explosive rise in all sorts of mental sicknesses and physical ones like cancer as seen in the authors generation. Also why eugenics popped up around the same time in a gung ho kinda way. The author did have a chapter on psychopathic-like cases that I found relatable. I was just on an SSRI at the time and no anti-inflammatories to boost my cognition when I read this, but I scored so many grades ahead in reading comprehension as a teen.

I think I was reading his last edition published in the 70's. The first case was a woman who just slept with men one time than broke off any attempt for a relationship. She said she saw her parents relationship as shallow and some kind of monotonous existence. He did help her to change, but her case screamed out at me as borderline or maybe a bit histrionic. Then the next case study was an engineer type who had been dating long term and he stated aloofly that he supposed they should get married. Not stating like he's passionately in love with her. That struck me as aspersers. Though I read somewhere that a small, but modest set of the population are really cerebral and not that emotional without meeting threshold I imagine for aspersers or any extra criterion. I read it 5 years ago, so I don't recall how many case studies there were. I remember one stumped me because it was so different from myself. But the case was a middle manager type or business man whom was able to meet responsibilities of his position but was prone to drink excessively or be unreliable in his personal life. That later struck me as undiagnosed adhd. he mentioned some creative artist types, perhaps as another example who care enough to create their artwork but have a lot of qualities probably seen as normal today, but less so in his day. Those types are just creative types with various personality disorders, I not an expert.

I believe non of these terms or diagnosis were part of the DSM in the 50-70's when the author held his career, or I could be mistaken. Perhaps a superficial-minor analysis I defiantly do not excel in understanding the human condition, ha ha. I just thought I'd point out the anti-social or unstable type disorders is pretty broad and diverse. For instance someone with OCPD may or may not come across as an army drill Sergeant type persona. That disorder has been debated to be moved to the unstable category from Anxious type. I am editing this on computer. I guess I may have had a reason to share this section, or maybe it just shows my interest and personal stake in mental health.

Edited by bullGenteel, 22 February 2026 - 08:14 PM.

[bullGenteel]

But back to schizophrenia theories:
I mentioned to galaxy in another thread about nicotine. This will be my 2 cents, but I did read about one paradigm lenses to look thru at psychosis as something that anyone could be diagnosed with. Its not super uncommon for people to get diagnosed in the past and they would convalesce in warmer weather climate for months at a time, if they were affluent lucky. I got this splice of a different perspective from a researcher I respect that I mentioned to Galaxy, so I will have to make a post about or share his blog. Perhaps others have heard the following statistics that perhaps 49% of people diagnosed with psychosis recover, but if they are put on anti-psychotics, then only 27% will still go on to make a full recovery. I am not positive these are the exact number, but it can support a different way to view the disorder. I should really type on the computer not my phone, but I am slow, either way based off being exposed to cigarettes smoke with resultant deficits mimicking ADHD or SCT. ( I am editing now with keyboard). I usually enjoy my own show, so I hope others do to. : )

I'm a pretty remedial person without any scientific knowledge or education. But I do wonder if OCD and psychosis may have a very similar disease profile. Likely there are different brain regions involved like Galaxy has proposed in this thread and other users I am sure. I don't see myself being able to delve into the science myself. I know intrusive thoughts in OCD are denoted as delusions. I know both diseases can be a very debilitating disorder causing people to be a recluse and/or institutionalized not being uncommon. I had a feeling that the unknown affliction Darwin suffered from when he cut ties with the world, except for his immediate family, maybe have been OCD, which is a little ha ha-funny, no disrespect intended, considering how he went super overboard in classifying animals in his natural selection/evolutionary framework. Lots of genius tend to have some from of schizophrenia, I believe JKR and a few others have OCD. One of the self titled smartest man in America I got it in my head or some anonymous person postulated he did. I am in no way a genius but I have parents whom likely is some kind of one and the other is bright average. Ha ha- why I wouldn't really ever deem myself to feel flattered, in comparison, if I was told I'm bright- I have some ideas what bright is, Mensa close brightness isn't anywhere near it.
Back to the comparison of OCD and psychosis:
Maybe I should try to keep this brief, since maybe in the future I'll be better the details to go along with any novel observations. I saw a Facebook post, yes FB, so sue me, theorized that a person's own thoughts become presented as visual or auditory hallucinations. I know from OCD it can be super disconcerting to deal with intrusive thoughts, especially in teen years when working memory is at its peak and social awkwardness is at its peak. The area of the brain that registers people surveying you is at its peak. I read a quick theory in this site that it may be the threat detection system is ramped up in OCD, so any possible bad outcome is constantly cycling in your head at times. It is known that the whatever made up stuff Freud came up with, a part of your psyche does judge yourself harshly. Perhaps that is magnified in OCD and psychosis much of the time.

I know the other poster in this thread mentioned at one time taking clozipine, I may be mistaken with the correct drug's name. But that researcher I mentioned and his colleague whose blogs I followed, mentions that clozipine would be the only medication he would endorse for psychosis, in place of any short term anti-psychotic or sedating agent to induce sleep to hopefully break a psychotic episode- or manic episode. The researcher stated clozapine is mildly sedating in its therapeutic action( I read this a few years ago), so it allows the patient to better ignore their delusions and function without all the horrible side effects of AP's. He did mention ECT because Robert, whoever swore by it, the Zen motor cycle philosofizer. I have a grandparent who may have benefited slightly from etc.

Jump ahead to my thinking along the lines of nicotine. If clozipine can mildly sedate one to function better thru pushing delusions or hallucinations from the forefront. Perhaps such an agent, or something that has similar therapeutic profile like sarcosane(I'm reaching/guessing with memory and working memory scores 20 points lower in IQ to other domains, ha ha); than such an agent, combined with nicotine could be complimentary in therapeutic potential. Since it may be that nicotine which is known to allow people to focus better may also allow both ocd and psychotic sufferers to normalize thru less intrusive thoughts/delusions to allow a switch in focus to some more regular in the moment mode of thinking that is contextually related more to what is the matter at hand . I know some therapies like desensitization can allow you to ignore intrusive thoughts. Perhaps if one was motivated like me it could be feasible to retrain your brain architecture to allow you to function a bit better with a combo I suggest. Who knows.

I know nicotine may help with depression to stop you to not drift away from the moment and fall into melancholic negative thinking. There is also depression with psychotic features. I know galaxy mentioned having addictive energies so nicotine may be out of consideration. Perhaps then one could combine it with buperion but that may be a reach.

So if you reframe how you approach to how you see the disorder, such is how I have been influenced into thinking by the two researchers I mentioned. Then you keep in mind that schizophrenia may involve high bdnf and can be a creative, perhaps more spiritually orientated manifestation. Yes I am sure it is very devastating at times to live with, especially with AP's thrown in, and same with OCD. You may look at it these conditions as something to be managed by augmenting the disorder to balance improved functioning thru more in the moment thinking with less distracting supplmentary cognitive processing. This would be benefical in contrast to try and obliterate all negative aspects, takeing away much functioning. Perhaps you could use some agent that slightly depresses the delusions as less needed additional overhead, background thinking. This refocusing onto more present, productive cognitive functioning could be then further set to the default with use something like nicotine that promotes focus. I am not the best at evaluating my ideas. I scored 20 points lower in logic/memory, but all the other domains were in the same higher range.

I think I will post the newer nicotine delivery agents being developed that I saw on my AI Google search. They use nitric oxide donating molecular combos, or what not to hopefully allow nicotine to do its thing, at same time relaxing the blood vessels walls. I suspect if it is possible than questforlife would be the candidate to reverse engineer such a pharma agent using known agents. I can be a naive optimist. I would be surprised if that is possible. Not to get peoples hopes up, so hopefully the vaping agents I researched, though not an health idea will be affordable and not too distantly to come down the pipeline pun intended. I don't think nicotine on its own is the answer as of yet.

Maybe this has some merit, others could decide or run with it. I only focus on one thing at a time in my state. I tried to offer up some hope, whether it is substantial or not, oh well, I tried at least. More some theorizing generally without the usual scientific rigor based on studies.

[Galaxyshock]

I agree OCD has similar properties as schizo disorders, in fact they often overlap:

 

"Schizophrenia and Obsessive-Compulsive Disorder (OCD) often overlap, with 12%–25% of schizophrenia patients experiencing clinically significant obsessive-compulsive symptoms (OCS). This comorbid state, sometimes termed "schizo-obsessive disorder," is associated with earlier psychosis onset, greater cognitive impairment, and increased severity of negative symptoms. Both disorders may share underlying neurobiological, genetic, and neurochemical dysfunction, particularly involving dopaminergic, serotonergic, and glutamatergic systems."

 

Clozapine unfortunately may worsen OCD symptoms, my guess it is the release of glutamate by Clozapine, although AI says it's the serotonin receptor antagonism:

 

"Clozapine, while the most effective antipsychotic for treatment-resistant schizophrenia, frequently causes or worsens obsessive-compulsive symptoms (OCS) or disorders (OCD) in up to 47% of users, significantly higher than other antipsychotics. These symptoms are often dose-dependent, arising from potent serotonin receptor antagonism. Management includes reducing the clozapine dose, switching to other antipsychotics, or adding SSRIs (e.g., fluvoxamine, sertraline) to manage the symptoms."

 

I have heard common painkiller medication Ibuprofen significantly reduces OCD symptoms for those with the disorder, Ibuprofen decreases glutamate levels so it could be that or the anti-inflammatory properties.