67 lines
4.4 KiB
Plaintext
67 lines
4.4 KiB
Plaintext
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Episode: 1294
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Title: HPR1294: Causes of Schizophrenia, neurochemical theory
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Source: https://hub.hackerpublicradio.org/ccdn.php?filename=/eps/hpr1294/hpr1294.mp3
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Transcribed: 2025-10-17 23:07:00
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---
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Music
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You
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Hello everybody, my name is Sig Flops and this is Label, and today we're going to
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be talking about schizophrenia. Miami diagnosis of schizophrenia has caused me to
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research a bit and I found several theories as to its cause, including neurochemical
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theory. I'm interested in this particular theory because all anticycotics
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work based on assumptions. Other theories include genetic theories, developmental
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theories, infectious and immune theories, nutritional theories,
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endocrine theories and stress theories. So I'm not a doctor right and this is my
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own interpretation of what's going on inside my head. Please don't take any of this
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as medical advice. Treatment of severe mental illness largely has been a
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guessing game with the discovery of therapies that seem to work, but with a little
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understanding of exactly how they work. It was discovered in the early 20th
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century that insulin coma therapy gives a 50-50 chance of people of a recovery
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where people schizophrenia. That's where the patient is given too much insulin
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and is actually put into a short-term coma. This is undoubtedly for several
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weeks until the patient becomes better. This is a standard practice of the medical
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establishment. Tell the discovery of thorazine, the first neuroleptic or
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antipsacetic drug. Schizophrenia today is largely treated with antipsacotics, so how
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do these antipsacotics work? The two major theories that dominate schizophrenia
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research from 1960s on are genetic theories and neurochemical theory.
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Neurochemical theory is primarily focused on neurotransmitters, which are the
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chemicals that carry messages between brain cells. Among the neurotransmitters is
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dopamine, which is primary focus of antipsacotic drugs. Thorazine was found to
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block dopamine, which is right awesome. The fetamine releases dopamine is found
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to cause schizophrenia like symptoms, so dopamine and too much of it is the name
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of the game. Well, not really. Some of the game antipsacotics today are grouped
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into what's called first-generation and second-generation antipsacotics. Only
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first-generation antipsacotics deal primarily with dopamine receptors and
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blocking them. The first-generation antipsacotics we've discovered are
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Haldol, Prolyxin, Nebine, Stylyoluzine, Chylophon, Loxetane, Mobine, Serenetil,
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Merilo, and Finely Thorazine. Second-generation antipsacotics deal with dopamine,
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while most of them, not all of them do, and other neurotransmitters.
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Glutamate, another neurotransmitter is an example of this. Much of the
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interest in glutamate stems from the fact that the street drug PCP causes schizophrenia
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like symptoms and also blocks glutamate. Glutamate is used in the brain to
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synthesize gamma-Meno-buretric acid, which is a major inhibitory neurotransmitter.
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There is considerable evidence that both glutamate and gamma-Meno-buretric acid
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are somehow involved in causation of schizophrenia. Other neurochemicals are
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being studied by schizophrenia researchers. A group of considerable interest is in
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the neuropeptides, which also acts as neurotransmitters. Second-generation
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antipsacotics include a lot of drugs, too many to, too many to list. Right now I'm
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on a couple of them, a bilify, which in high doses is an antipsacotic and
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risk-bridle. My personal theory of schizophrenia is that there is a genetic
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structure of the brain, which gives a predisposition towards developing schizophrenia,
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and it's the neurotransmitters that trigger it. A new medical evidence to
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support this, it's just my feeling. Thanks for listening, everyone, and take
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care.
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