Episode: 1294
Title: HPR1294: Causes of Schizophrenia, neurochemical theory
Source: https://hub.hackerpublicradio.org/ccdn.php?filename=/eps/hpr1294/hpr1294.mp3
Transcribed: 2025-10-17 23:07:00

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