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Post by flyingcarpet46 on Jun 18, 2022 5:50:45 GMT
Current research. What do you think my two posts on serontonin and dopamine were ?
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Post by flyingcarpet46 on Jun 18, 2022 6:02:06 GMT
Weii, i guess 2014/15 is out of date but I expect ncbi (Natioal.Centre of Biotechnology) to be teasomably up to date.
And these two articles were at least nuanced. Give me later research and I'll look at it.
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Post by flyingcarpet46 on Jun 18, 2022 6:05:55 GMT
But I did the reasonable thing for someone in my situation. Did a google search and looked for reasonable posts. You are being unreasonable.
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Post by flyingcarpet46 on Jun 18, 2022 6:25:00 GMT
OK 2020. www.ncbi.nlm.nih.gov/pmc/articles/PMC6953551/Dopamine and glutamate in schizophrenia: biology, symptoms and treatment Robert A. McCutcheon, John H. Krystal, and Oliver D. Howes ABSTRACT Glutamate and dopamine systems play distinct roles in terms of neuronal signalling, yet both have been proposed to contribute significantly to the pathophysiology of schizophrenia. In this paper we assess research that has implicated both systems in the aetiology of this disorder. We examine evidence from post‐mortem, preclinical, pharmacological and in vivo neuroimaging studies. Pharmacological and preclinical studies implicate both systems, and in vivo imaging of the dopamine system has consistently identified elevated striatal dopamine synthesis and release capacity in schizophrenia. Imaging of the glutamate system and other aspects of research on the dopamine system have produced less consistent findings, potentially due to methodological limitations and the heterogeneity of the disorder. Converging evidence indicates that genetic and environmental risk factors for schizophrenia underlie disruption of glutamatergic and dopaminergic function. However, while genetic influences may directly underlie glutamatergic dysfunction, few genetic risk variants directly implicate the dopamine system, indicating that aberrant dopamine signalling is likely to be predominantly due to other factors. We discuss the neural circuits through which the two systems interact, and how their disruption may cause psychotic symptoms. We also discuss mechanisms through which existing treatments operate, and how recent research has highlighted opportunities for the development of novel pharmacological therapies. Finally, we consider outstanding questions for the field, including what remains unknown regarding the nature of glutamate and dopamine function in schizophrenia, and what needs to be achieved to make progress in developing new treatments. IF YOU AND I WERE EACH TO JIGHLIGHT THIS ARTICLE , we would highlight different sections.
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Post by flyingcarpet46 on Jun 18, 2022 6:54:15 GMT
2018
Review Article Open Access Published: 31 January 2018 Dopamine, psychosis and schizophrenia: the widening gap between basic and clinical neuroscience JP Kesby, DW Eyles, …JG Scott Show authors Translational Psychiatry volume 8, Article number: 30
Introduction
Our knowledge of the neurobiology of schizophrenia, ** while still rudimentary ** has advanced considerably in recent years.
However,these findings have not translated to better treatments for those with schizophrenia
The three primary symptom groups, positive, cognitive and negative (Box 1), have been associated with reports of abnormalities in virtually every neurotransmitter system1,2,3,4,5.
The onset of psychotic symptoms, which is strongly associated with alterations in dopamine function, is a key feature underpinning a clinical diagnosis6, 7. However, results from clinical research regarding the specific loci of dopamine dysfunction in schizophrenia8,9,10, have triggered a reappraisal of our perspective on the neurobiology of schizophrenia.** Currently there is a disparity between the tests for positive symptoms in animal models and recent clinical evidence for dopaminergic abnormalities in schizophrenia **
Therefore, it is critical that this contemporary clinical knowledge actively influences the agenda in applied basic neuroscience. ....
It is widely acknowledged that we cannot recreate the complicated symptom profile of schizophrenia in animal models. However, animal models (the majority and focus of the present article being rodent models) provide an avenue to invasively explore the role of neurotransmitters and circuitry in psychiatric diseases.
To improve the ** poor predictive validity of treatments in animal models11, it is critical that our understanding and the use of animal models evolves alongside our knowledge of schizophrenia neurobiology **The delayed incorporation of new clinical findings to develop better animal models highlights the need for better communication between clinical and basic research communities.
In this article, we discuss the challenges clinicians and researchers are facing in understanding the neurobiology of positive symptoms and psychosis in schizophrenia. We discuss the implications this has for current assessments of positive symptoms in rodents and propose a more relevant set of tests for future study.
Finally, the need for a joint focus on bi-directional translation between clinical and basic research is outlined.
Challenges in diagnosing schizophrenia Psychiatric symptoms exist on continua from normal to pathological, meaning ** the threshold for diagnosis of schizophrenia in clinical practice can be challenging.**
The clinical diagnosis of schizophrenia relies heavily on the positive symptoms associated with a prolonged psychotic episode. However, a relatively high percentage of the general population (8–30%) report delusional experiences or hallucinations in their lifetime12,13,14, but for most people these are transient15. Psychotic symptoms are also not specific to a particular mental disorder16.
The clinical efficacy of antipsychotic drugs is heavily correlated with their ability to block subcortical dopamine D2 receptors17, 18, suggesting dopamine signalling is important. In spite of this,** no consistent relationship between D2 receptors and the pathophysiology of schizophrenia has emerged19, 20. ** In contrast, the clinical evidence points towards presynaptic dopamine dysfunction as a mediator of psychosis in schizophrenia19.
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Post by flyingcarpet46 on Jun 18, 2022 7:04:34 GMT
2022
Do high dopamine levels cause schizophrenia? High levels of dopamine don’t cause schizophrenia symptoms. The role dopamine plays in schizophrenia is more complex than that and involves specific dopamine activity.
Over time, researchers have discovered evidence that isn’t in line with the original dopamine hypothesis of schizophrenia. For example, they found that some people with schizophrenia had typical levels of dopamine in their cerebrospinal fluid as opposed to elevated levels.
Further, researchers found that other antipsychotic drugs that do not block the effects of dopamine could still treat symptoms of schizophrenia.
Some schizophrenia symptoms may be triggered when certain areas of the brain have high levels of dopamine activity while others have lower levels of activity.
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Post by flyingcarpet46 on Jun 18, 2022 7:08:35 GMT
2022 However, it's also important to remember that schizophrenia is a complex disorder, and there are many ways the disease can manifest. Dopamine hyperactivity may not be the primary cause of schizophrenia in all patients. Furthermore, even if dopamine hyperactivity is the primary cause it still doesn't explain why some patients respond more strongly than others to the same treatment. www.verywellmind.com/the-relationship-between-schizophrenia-and-dopamine-5219904
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Post by flyingcarpet46 on Jun 18, 2022 8:45:07 GMT
I was prescribed Largatil, first generation antipsychotic
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Post by flyingcarpet46 on Jun 18, 2022 8:54:56 GMT
Largatil - thorazine - chlorpromazine
Is also a dopamine antagonist.
Chlorpromazine is in the typical antipsychotic class,[4] and, chemically, is one of the phenothiazines. Its mechanism of action is not entirely clear but believed to be related to its ability as a dopamine antagonist.[4] It also has anti-serotonergic and antihistaminergic properties.[4]
Common side effects include movement problems, sleepiness, dry mouth, low blood pressure upon standing, and increased weight.[4] Serious side effects may include the potentially permanent movement disorder tardive dyskinesia, neuroleptic malignant syndrome, severe lowering of the seizure threshold, and low white blood cell levels.[4] In older people with psychosis as a result of dementia it may increase the risk of death.[4] It is unclear if it is safe for use in pregnancy.[4]
Chlorpromazine was developed in 1950 and was the first antipsychotic on the market.[5][6] It is on the World Health Organization's List of Essential Medicines.[7][8] Its introduction has been labeled as one of the great advances in the history of psychiatry.[9][10] It is available as a generic medication.[4]m
I didnt take well to this medication - and when I was prescribed it no one explained the side effects.
IN MY VIEW ALL MEDICATIONS SHOULD BE TREATED WITH CAUTION AS TO HOW THEY WORK WHICH IS NOT TO DENY THE CONDITIONS/SYMPTOMS THEY ARE DESIGNED TO EASE.
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Post by Admin on Jun 18, 2022 8:57:02 GMT
Converging evidence indicates that genetic and environmental risk factors for schizophrenia underlie disruption of glutamatergic and dopaminergic function. However, while genetic influences may directly underlie glutamatergic dysfunction, few genetic risk variants directly implicate the dopamine system, indicating that aberrant dopamine signalling is likely to be predominantly due to other factors. Hence integral.
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Post by Admin on Jun 18, 2022 9:33:46 GMT
IN MY VIEW ALL MEDICATIONS SHOULD BE TREATED WITH CAUTION AS TO HOW THEY WORK WHICH IS NOT TO DENY THE CONDITIONS/SYMPTOMS THEY ARE DESIGNED TO EASE. Yes - all medications should be treated with caution. Far more focus, help & support should be on the psychological, social & spiritual elements of mental health, while also not denying the biological elements & the realities of mental illnesses.
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Post by flyingcarpet46 on Jun 18, 2022 9:42:16 GMT
I think dual diagnosis places you in a partially separate grouo esp re severity.
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Post by flyingcarpet46 on Jun 18, 2022 9:48:21 GMT
On your integral model. We've discussed that quite a few tines including quite recently.but it's clear we won't see to eye.
Your integral model appears as an abstraction on ,as used to be said, the back of an envelope. Detail is needed both on what provision is needed, how this might be met and implemented.
But your model is a good starting place but the issye remains on which details are/not negotiable /open to modification.
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Post by Admin on Jun 18, 2022 9:48:56 GMT
I think dual diagnosis places you in a partially separate grouo esp re severity. i think it does yes - but it's also not complicated to see that someone is suffering from addiction & mental illness & it accounts for 50% of cases - it is a major issue in society & not unusual. Far more should be done for dual diagnosis disorders. & we should move away from the moralizing / blame & crime & punishment approaches.
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Post by Admin on Jun 18, 2022 9:56:32 GMT
On your integral model. We've discussed that quite a few tines including quite recently.but it's clear we won't see to eye. Your integral model appears as an abstraction on ,as used to be said, the back of an envelope. Detail is needed both on what provision is needed, how this might be met and implemented. But your model is a good starting place but the issye remains on which details are/not negotiable /open to modification. No one is going to agree on the religion / spirituality question. No one is going to agree on psychological models of the mind - there are over 120 different schools of psychology. No one is going to agree on how the hard & soft science & science & spirituality should be integrated. No one is going to agree on how mental health acts / laws should be designed & implemented. No one is going to agree on what severe mental illness is / isn't - it's causes, & how it should best be treated. No one is going to agree on the various integral / holistic models that are out there. No one is going to agree on politics / socioeconomics & civilizational / social systems. No one is going to agree on anything - & we shall carry on with all the same mess into increasing global ecological & civilizational Collapse likely until all humans & most life on the planet is dead.
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