Dopamine reward system > IQ

zombie

Rotting until the day I am actually dead
Rotters
Joined
May 12, 2018
Messages
5,780
Reputation
2,289
Dopamine like every other neurotransmitter needs balance, excess is just as harmful as a deficiency of it.
 

freethinker

Jock
Oldcels
Joined
Aug 31, 2018
Messages
1,335
Reputation
443
IQ is so overrated. Sure if you want to stemmaxx it's useful but otherwise it just seems like a fucking burden. Most legit high IQ people i know are "off" in some way and everyone agrees with that assessment.

You don't need a high spatial reasoning ability or whatever to succeed in life. Much rather be pretty or high dopamine.
 

boojies

Certified genius
Joined
May 5, 2019
Messages
994
Reputation
12
psychosis is a chad trait @boojies @fuckgoebbelz @mrz
The dopamine hypothesis of schizophrenia didn't end up panning out so well. Today the NMDAR hypofunction hypothesis has attracted the most interest.


I only started studying matters after research had progressed to largely rejecting the dopamine hypothesis and had started focusing on the NMDAR hypofunction hypothesis though, so I am not that familiar with the more classical research.
 
Last edited:

phuckthisgayearth

Super Lookism.net Creator
Staff member
Joined
Mar 19, 2018
Messages
9,358
Reputation
1,568
The dopamine hypothesis of schizophrenia didn't end up panning out so well. Today the NMDAR hypofunction hypothesis has attracted the most interest.


I only started studying matters after research had progressed to largely rejecting the dopamine hypothesis and had started focusing on the NMDAR hypofunction hypothesis though, so I am not that familiar with the more classical research.
true, but it's not like dopamine doesn't cause a lot of the positive symptoms, it's just that glutamatergic and dopaminergic systems are related, with the glutamatergic/nmda dysfunction being closer to the root of the issue in schizophrenia; dopaminergic stimulants alone can definitely still cause psychosis, so oldmate above is right in essence that too much dopamine will make you batshit crazy ie. a gigachad
 

boojies

Certified genius
Joined
May 5, 2019
Messages
994
Reputation
12
I suppose they do use dopamine antagonists for treating schizophrenia, so that indicates that the people prescribing such things for schizophrenia still have some degree of belief in the dopamine hypothesis. It could just take decades for the old wisdom to work its way through our society though -- hard to say. There is a lot of old research in support of the dopamine hypothesis, but before that I think it was the serotonin hypothesis. Then again


SiteKi (nM)Action
5-HT1A423Antagonist
5-HT1B14.9Antagonist
5-HT1D84.6Antagonist
5-HT2A0.17Inverse agonist
5-HT2B61.9Inverse agonist
5-HT2C12.0Inverse agonist
5-HT5A206Antagonist
5-HT62,060Antagonist
5-HT76.60Irreversible
antagonist[41]
α1A5.0Antagonist
α1B9.0Antagonist
α2A16.5Antagonist
α2B108Antagonist
α2C1.30Antagonist
D1244Antagonist
D23.57Antagonist
D2S4.73Antagonist
D2L4.16Antagonist
D33.6Inverse agonist
D44.66Antagonist
D5290Antagonist
H120.1Inverse agonist
H2120Inverse agonist
mACh>10,000Negligible
they still do treat it with inverse serotonin agonists / serotonin antagonists, which would just as much so indicate a potential continued adherence to the serotonergic hypothesis of schizophrenia. The modern treatments -- last I knew -- was going through clinical trials still, and they are NMDAR positive allosteric modulators, which indicates a coming around to the NMDAR hypofunction hypothesis. How discouraging that the history of schizophrenia treatment has been one of consistent hope and disappointment.


Schizophrenia is a serious psychiatric illness that is responsible for a substantial proportion of mental illness worldwide. Symptoms include hallucination, delusions, thought disorder and negative symptoms, including poverty of thought and emotion, and social withdrawal. Early theories of schizophrenia implicated disturbed serotonin (5-HT) neurotransmission, but these were largely overshadowed by the dopamine theory of schizophrenia, which became established after the introduction of chlorpromazine.
https://www.cell.com/fulltext/S0896-6273(03)00757-8

The introduction of several new antipsychotic drugs in the last decade promised to treat schizophrenia more efficaciously than conventional antipsychotics, and without the unwanted side effects. These drugs, which were modeled after clozapine, reduce dopamine receptor function. However, a discouraging outcome of treatment with these drugs is emerging: they do not substantially improve clinical outcome for schizophrenia and, worse, some produce dangerous side effects, such as weight gain, diabetes, and elevations in blood lipids.

Over the past two decades, accumulating evidence has implicated the role of glutamatergic dysfunction in the pathophysiology of schizophrenia. There has been growing interest in glutamatergic system as a promising target for treatment of schizophrenia spectrum illness and several medications and compounds have been investigated to date. In the present study, we aim to provide a comprehensive review of clinical studies of glutamatergic agents in treatment of schizophrenia. We further discuss the heterogeneity of the results, the overall discouraging outcomes and future directions for investigating glutamatergic medications in schizophrenia.
The heterogeneity of results isn't that surprising to me. Schizophrenia is thought today to be a set of phenotypes, each of which having an autistic inversion. As a set of distinct phenotypes, it's pretty much tautological that it is a heterogeneous condition.


Liemburg et al40 studied connectivity within the DMN and hypothesized that poor-insight patients (n=19) would show greater connectivity impairment than their good-insight peers (n=25). Insight grouping was assigned on the basis of the PANSS insight item (G12). All subjects underwent resting fMRI. Results showed that “schizophrenia patients with relatively preserved insight showed stronger connectivity than patients with poor insight in the anterior cingulate cortex and precuneus, both key regions in self-reflective processing. These findings tentatively support the hypothesis that poor insight may be related to impaired self-related processing.” In other words, poor insight was associated with a relative breakdown of DMN connectivity and operations.

Orfei et al30 used the BCIS along with structural and diffusion tensor MRI neuroimaging techniques (latter to inspect white matter architectural organization) to study the neuroanatomy of cognitive insight in schizophrenia, comparing 45 patients with schizophrenia to 45 healthy control subjects. The results showed a correlation between insight as measured by the BCIS self-reflectiveness index and lower gray matter volume in the right ventrolateral prefrontal cortex (VLPFC). The VLPFC is involved in working memory and decision making. The findings suggest that a reduced VLPFC volume corresponds with a diminished capacity to entertain alternative explanations about one’s misperceptions leading to impairment in awareness of illness.
Those are both neurological presentations associated with schizophrenia; however, they are not equivalent. The breakdown of the default mode network is associated with clinical insight deficits; the reduced volume of the vlpfc with cognitive insight deficits.


There are self-administered, validated tools as well, such as the Beck Cognitive Insight Scale (BCIS),11 which is based on a separation of the concepts of “cognitive insight” and “clinical insight.” Clinical insight is described as the awareness of mental illness requiring treatment, while cognitive insight encompasses the patient’s ability to evaluate, reappraise, and modify distorted beliefs or misperceptions. These interpretations are regulated at a “higher level” of cognition, also called metacognition, allowing clinicians to assess self-regulating and self-monitoring functions of thought processes. The BCIS assesses a patient’s objectivity about delusional thinking, previous errors, reattribution of false explanations, and ability to receive corrective information from others. It includes self-reflectiveness and self-certainty subscales in order to measure willingness and capacity to entertain alternate explanations and over-confidence in validity of beliefs.
I would only expect the NMDAR PAMs to work in cases with diminished vlPFC volume, for they essentially will serve to strengthen one of the primary functions of the vlPFC -- maintaining activation of the task positive network despite emotional distractions in the environment.


The ventrolateral prefrontal cortex (vlPFC) is a subdivision of the prefrontal cortex. Its involvement in modulating existing behavior and emotional output given contextual demands has been studied extensively using cognitive reappraisal studies and emotion-attention tasks. Cognitive reappraisal studies indicate the vlFPC’s role in reinterpreting stimuli, and reducing or augmenting responses. Studies using emotion-attention tasks demonstrate the vlFPC’s function in ignoring emotional distractions while the brain is engaged in performing other tasks.[6]https://en.wikipedia.org/wiki/Inter..._executive_brain_systems#cite_note-mitchell-6
In schizophrenia with normal vlPFC volume but lesioning of the default mode network, I wouldn't expect improvement from NMDAR PAMs.


A prominent feature of the human brain’s global architecture is the anticorrelation of default-mode vs. task-positive systems. Here, we show that administration of an NMDA glutamate receptor antagonist, ketamine, disrupted the reciprocal relationship between these systems in terms of task-dependent activation and connectivity during performance of delayed working memory. Furthermore, the degree of this disruption predicted task performance and transiently evoked symptoms characteristic of schizophrenia.

Whitfield-Gabrieli et al39 studied patients with schizophrenia; young, at-risk, first-degree relatives; and unaffected controls using fMRI during alternating conditions of wakeful rest and a focused working memory task. While the unaffected controls showed predictable deactivation of DMN during active task, the patients and relatives showed diminished deactivation, as well as greater activity in right DLPFC. This finding has essentially been replicated twice by two other research groups.
I would expect that group of schizophrenics -- with diminished deactivation of the default mode network during working memory task -- to be the one that benefited from the NMDAR positive allosteric modulators.
 
Last edited:

itsoverkillyourself

half vietnamese dark triad badboy
Joined
Jan 1, 2020
Messages
749
Reputation
208

phuckthisgayearth

Super Lookism.net Creator
Staff member
Joined
Mar 19, 2018
Messages
9,358
Reputation
1,568
I suppose they do use dopamine antagonists for treating schizophrenia, so that indicates that the people prescribing such things for schizophrenia still have some degree of belief in the dopamine hypothesis. It could just take decades for the old wisdom to work its way through our society though -- hard to say. There is a lot of old research in support of the dopamine hypothesis, but before that I think it was the serotonin hypothesis. Then again




they still do treat it with inverse serotonin agonists / serotonin antagonists, which would just as much so indicate a potential continued adherence to the serotonergic hypothesis of schizophrenia. The modern treatments -- last I knew -- was going through clinical trials still, and they are NMDAR positive allosteric modulators, which indicates a coming around to the NMDAR hypofunction hypothesis. How discouraging that the history of schizophrenia treatment has been one of consistent hope and disappointment.




https://www.cell.com/fulltext/S0896-6273(03)00757-8






The heterogeneity of results isn't that surprising to me. Schizophrenia is thought today to be a set of phenotypes, each of which having an autistic inversion. As a set of distinct phenotypes, it's pretty much tautological that it is a heterogeneous condition.







Those are both neurological presentations associated with schizophrenia; however, they are not equivalent. The breakdown of the default mode network is associated with clinical insight deficits; the reduced volume of the vlpfc with cognitive insight deficits.




I would only expect the NMDAR PAMs to work in cases with diminished vlPFC volume, for they essentially will serve to strengthen one of the primary functions of the vlPFC -- maintaining activation of the task positive network despite emotional distractions in the environment.




In schizophrenia with normal vlPFC volume but lesioning of the default mode network, I wouldn't expect improvement from NMDAR PAMs.







I would expect that group of schizophrenics -- with diminished deactivation of the default mode network during working memory task -- to be the one that benefited from the NMDAR positive allosteric modulators.
what i meant is that i was under the impression that nmdar hypofunction causes the positive symptoms mostly because nmdar regulates dopamine function (hence dopaminergic drugs coming with a risk of psychosis), and that in that sense the two theories are more complimentary than exclusive, and afaik clozapine et al does generally work well for positive symptoms, the reason they aren't great for clinical outcomes is because they make the negative symptoms (ie. laziness, anhedonia, braindeadness) worse, just ask mvp, he's living that reality right now

but maybe im wrong, idk, i'll defer to you since understanding the schizo brain is one of your life missions
 

boojies

Certified genius
Joined
May 5, 2019
Messages
994
Reputation
12
One thing to keep in mind is that psychosis is a symptom; conversely, schizophrenia is a condition that presents with psychosis. I'm not very familiar with the dopamine mechanism for psychosis, but amphetamine increase synaptic dopamine (as a dopamine releasing agent, it causes the synaptic vesicle of a dopamine neuron to release its neurotransmitter into the synapse).


Infusions of the dopamine releasing agent amphetamine or the dopamine uptake inhibitor nomifensine resulted in a dose-dependent increase in the overflow of dopamine.
and it is known that it can cause -- at least acute -- psychosis.


Amphetamines may induce symptoms of psychosis very similar to those of acute schizophrenia spectrum psychosis. This has been an argument for using amphetamine-induced psychosis as a model for primary psychotic disorders. To distinguish the two types of psychosis on the basis of acute symptoms is difficult. However, acute psychosis induced by amphetamines seems to have a faster recovery and appears to resolve more completely compared to schizophrenic psychosis.
However, amphetamine likely causes deactivation of the default mode network,


Conclusions/Significance

These findings provide evidence that dopamine transporters modulate neural activity in the DMN and anterior cingulate gyrus during visuospatial attention. Our findings suggest that dopamine modulates attention in part by regulating neuronal activity in posterior parietal cortex including precuneus (region involved in alertness) and cingulate gyrus (region deactivated in proportion to emotional interference). These findings suggest that the beneficial effects of stimulant medications (increase dopamine by blocking DAT) in inattention reflect in part their ability to facilitate the deactivation of the DMN.

Zhou et al.109 found evidence for increased resting state connectivity in the DMN in a schizophrenic group, along with increased anticorrelation between the DMN and another brain network known as the task-positive network (TPN). Such anticorrelations are found in healthy individuals110 and are thought to reflect the ongoing switching of attention between the external and internal words, mediated respectively by the TPN and DMN.


Is a sort of artist's conception I've fashioned.




Schizophrenia is waking reality processed through the dreaming brain

In contrast to the default mode network-like activation patterns of normal REM sleep , brain regions activated during lucid dreaming comprise substantial parts of the frontoparietal control network .
It's massively complex and hard to think of though. It's hard to reconcile amphetamine inducing a psychosis similar to schizophrenia's with amphetamine (probably) causing diminished activation of the default mode network. I find that it is really cognitively demanding trying to process all of the pertinent information into a coherent whole. There is just such nuance to neuropsychiatry, and so much inversion that it makes my head spin. It's amazing how essentially inverted conditions can both present as one condition (the extreme ends of the autism-psychosis spectrum being two states of catatonia that have been difficult for the researchers to tease apart).
 

averagefailednormie

Slayer
Escortcels
Joined
Jan 10, 2020
Messages
3,485
Reputation
1,367
One thing to keep in mind is that psychosis is a symptom; conversely, schizophrenia is a condition that presents with psychosis. I'm not very familiar with the dopamine mechanism for psychosis, but amphetamine increase synaptic dopamine (as a dopamine releasing agent, it causes the synaptic vesicle of a dopamine neuron to release its neurotransmitter into the synapse).




and it is known that it can cause -- at least acute -- psychosis.




However, amphetamine likely causes deactivation of the default mode network,









Is a sort of artist's conception I've fashioned.









It's massively complex and hard to think of though. It's hard to reconcile amphetamine inducing a psychosis similar to schizophrenia's with amphetamine (probably) causing diminished activation of the default mode network. I find that it is really cognitively demanding trying to process all of the pertinent information into a coherent whole. There is just such nuance to neuropsychiatry, and so much inversion that it makes my head spin. It's amazing how essentially inverted conditions can both present as one condition (the extreme ends of the autism-psychosis spectrum being two states of catatonia that have been difficult for the researchers to tease apart).
didnt read
 
Joined
Sep 27, 2017
Messages
5,186
Reputation
889
I have IQ in 140’s. The answer is a definite yes.

Studies show the higher your IQ, the higher risks for mental illness, anxiety, and severe depression. Because you can objectively see yourself. Like the saying goes, “you require an immense amount of knowledge just to be able to see your own depth of ignorance.” This is probably going to be a long and involved answer, so please stick with me.

Your ego is a mask, a story that you tell yourself. But those with high IQ are more easily able to see through the mask, and without some sort of spirituality, there’s nothing underneath. When you see your ego is false, it’s like a mirror looking into a mirror. But the up side is that you can see how your subconscious is programmed and take control of the 95% subconscious actions that we all have.

But because you see right through your ego…you also see straight through everyone else’s! If you’re not careful to agree with the subconscious lies everyone tells themselves, you WILL DEEPLY offend everyone. No one wants to hear that their problems today are the result of their actions and words yesterday, even if it’s as clear as day. They just want to be told they’re unlucky and have no control. You must realize what others want to believe is their life, and it’s not up to you to tell them the truth if they don’t want to see it.

If your IQ is too high for those surrounding you, you WILL be seen as insane, and highly ignorant. Because others don’t understand you, they assume you must be insane. They assume since you tell them stuff against their beliefs that you’re the one who’s ignorant. And they WILL HATE THE HELL OUT OF YOU! Intelligence must be hidden as much as possible for the sanity of the person who holds it. If you’re not careful, you’ll start to believe that you may just be insane and that will lead to many self destructive behaviors and thoughts. You must act dumb in many situations. (Anyone intelligent will see that I am putting a lot of emphasis on this, and usually our actions are the result of strong emotions, therefore I must have been extremely hurt recently or traumatized in the past by this lesson)

You rarely conform to social norms because they’re just stupid and a waste of time. This gets back into the ego I talked about. Almost 95% of our actions every single day are subconscious and random, depend on how society programmed our subconscious to respond to stimuli, and our ego justifies them after we do them in an effort to maintain consistent story. “I must have done that because I felt..” because few understand this, they think their programmed responses are free will, that they’re making the choice, even though science shows they react before they even have a mental thought. The thought and justification come after, sometimes by several seconds. The justification depends on what they’ve been programmed to believe to conform with their personal narrative. Society is brainwashed into thinking they need all these things to be happy, must be and act certain ways, even if they’re self-destructive. So the higher the IQ, the less you’re usually accepted by society.

The benefits are an insane ability to learn and master anything and pattern recognition. Pattern recognition is our superpower, and it leads us to see that much of society are not conscious. They don’t see that their lives are a reflection of their daily habits. Like going to the gym. They think becoming wealthy is luck, and has nothing to do with their daily learning and work. That’s like thinking someone going to the gym for two years just happened to luck out when they lost 50lbs on the way….They cannot see the correlation between using their turn signals and risks of accidents, or that how they react to others actually affects their lives. They live largely asleep. But when you see those patterns, that the entire universe revolves around magnificent and brilliant patterns, even human psychology, you generally have an extremely easy time manipulating those patterns to gain what you want or to help others. Wealth is easy.
 

averagefailednormie

Slayer
Escortcels
Joined
Jan 10, 2020
Messages
3,485
Reputation
1,367
This thread is flawed. Formative experiences determine your ability to have fun around normies. A lot of people here don't fit in with normies because of years of bad treatment due to our looks.
 

PsychoSocial

Escortcels
Joined
Dec 20, 2019
Messages
1,410
Reputation
739
One thing to keep in mind is that psychosis is a symptom; conversely, schizophrenia is a condition that presents with psychosis. I'm not very familiar with the dopamine mechanism for psychosis, but amphetamine increase synaptic dopamine (as a dopamine releasing agent, it causes the synaptic vesicle of a dopamine neuron to release its neurotransmitter into the synapse).




and it is known that it can cause -- at least acute -- psychosis.




However, amphetamine likely causes deactivation of the default mode network,









Is a sort of artist's conception I've fashioned.









It's massively complex and hard to think of though. It's hard to reconcile amphetamine inducing a psychosis similar to schizophrenia's with amphetamine (probably) causing diminished activation of the default mode network. I find that it is really cognitively demanding trying to process all of the pertinent information into a coherent whole. There is just such nuance to neuropsychiatry, and so much inversion that it makes my head spin. It's amazing how essentially inverted conditions can both present as one condition (the extreme ends of the autism-psychosis spectrum being two states of catatonia that have been difficult for the researchers to tease apart).
Genius
 

Moneycel

Coper
Joined
Jan 14, 2020
Messages
659
Reputation
239
Isn't this the majority of the losers who follow Aaron Clareys videos lol. A few select of my friends approach life in this way and it is getting them places. Having the motive and drive to constantly achieve new things is something a few people actually have. Most people just want to sit on their asses and complain about shit all day because their dopamine is fucked. Its the same with alcoholics, the same reason alcoholics always turn back to drink is because of the rewarding feeling they get from booz however people who do this via dopamine are succesful
 

Moneycel

Coper
Joined
Jan 14, 2020
Messages
659
Reputation
239
Your dopamine system isn't black and white like that. I have an IQ of 132, because of the way my dopamine system worked throughout my youth.

Some kids push themselves to the limit in social interactions, sports etc. I did the same, but at school when I was making calculations, giving presentations, etc. Always trying to be the best, pushing myself to the limit, going beyond the assignment. This is what got me the high IQ in the first place.

And that's exactly what got me fucked up, since kids hate smart kids. And being smart doesn't make you attractive, therefore getting you a negative halo and fucking up your social status.
Another twat who thinks hes smarter than he is blaming others for his downfalls. Delusional confirmed.
 
Top