This theory offers a compelling shift from dopamine-centric models to a more holistic, metabolic understanding of schizophrenia's sensory origins. While it provides a logical link between brain function and systemic health, it still requires rigorous empirical validation to move beyond a bold hypothesis.
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This Student Researcher May Have Discovered Something Huge.🌍🧠Added:
I bet you don't want to miss this one.
Watch this clip, guys.
Okay, I have to be quick. I'm pretty sure I just figured out another theory as to why patients have schizophrenia.
Okay, right now they have theories, but they don't actually have an answer, and I'm pretty sure I just discovered the [ __ ] answer, right? We had to do a research paper of our choice, and I chose schizophrenia. Going down this rabbit hole, I'm pretty sure I just put the pieces together. So, right now the theories they mostly focus on the amygdala and the hippocampus. Everybody knows the amygdala. The hippocampus focuses on memory recall. It is specifically there to help you remember [ __ ] but it is not specifically the first core connector when you gather new information. When you gather new information, you form a new thought. You have new information from your environment. Somebody's talking to you, anything else like that. That specifically goes through the thalamus first. Then, once it is done cycling through the thalamus, basically see your thalamus as like like a post office, right? So, you're receiving all these letters, all these pulses, and then it processes it through the neurons inside of it because there are so many neurons inside of there, and then it transfers it, and it takes it to whatever part of the brain that it needs to, correct?
Inside the thalamus, you have the glutamus, and the glutamus is basically 80% of it is compiled of glucose. And when you hear glucose, what do you hear?
You hear diabetes, right? You look at the the glucose levels within patients that have schizophrenia, their their levels are all over the [ __ ] place, right? That's why they're at higher risk of developing diabetes if you have schizophrenia. Okay? The antipsychotics that are being provided to these patients do not focus on glucose whatsoever. They kind of act like acetaminophen, like Tylenol almost.
So, Tylenol blocks pain receptors, right? Whereas the typical antipsychotics, they focus on dopamine, right? They focus on the dopamine receptors, but they don't actually help out with the leak inside of the thalamus with the glucose, okay? So, this metabolic gap essentially it's these antipsychotics, they disrupt the glucose regulation as a side effect. So, essentially, they're putting a band-aid over it similar as to how Tylenol does, but if they were to actually look into thalamus and regulate their glucose levels, I'm curious as to see how that would react to them. So, for example, certain medications such as and I might butcher these, olanzapine or olanzapine and clo- clozapine, right? Those are some of the most common ones provided to these patients and it specifically just targets dopamine. It does not target the thalamus in any form or fashion. So, these actually increase peripheral glucose, which this blockage leads to higher blood sugar and insulin resistance, which is why they're more more likely to develop diabetes, right?
And then they it impairs a brain sensing, so it blocks the brain's ability to sense sugar levels preventing it from adjusting metabolism correctly and glutamate reduction is also within that. So, basically, it's it's [ __ ] up the glucose all the way. When the glucose is something that needs to be [ __ ] repaired. When the glucose is something that needs to be looked at for the glutamate and the thalamus. Over 80% of the brain's glucose consumption is used to power the glutamate inside of the thalamus. If this is disrupted, you see lack of energy, you see build up of extra glutamate, which also often overwhelms the thalamic reticular nucleus or the TRN, and it causes that leak inside the sensory filter. I'm I'm reading my notes here.
I'm I'm doing a research paper. This disruption, this lack of stability within the glucose and this inside the glutamate is a direct correlation with the hallucinations. Also goes into effect for social withdrawal as well and a bunch of other symptoms that they develop, but the thalamus is the first thing that, you know, is in control of the information. So, it communicates to the hippocampus. It communicates to the amygdala. They do not communicate first unless you are specifically calling back to a memory, okay? While gray matter regions in the thalamus may show decreased use, some research indicates that higher metabolic rates in white matter tracts connecting the thalamus to the cortex. This insufficiency model suggests that the brain is working harder to relate poorly regulated or leaky information. When your thalamus is leaking information, it's not able to process, it's not able to communicate everything as it's supposed to, or it's being overwhelmed with information and it's basically blocked. Okay? That is what is causing the the hallucinations.
That is what is causing it, right? So, let me ask you this. When you are alone in a dark room, you don't have any sound, you don't have your phone, you have literally nothing, just you in a dark room, what happens?
Your brain creates stories. Your brain makes you see [ __ ] It makes you hear [ __ ] You can literally give yourself hallucinations. That's often why a lot of people are scared of the dark, right?
It's all in the mind. And so, basically, these patients are basic they're in like a waking realm. So, basically, they're like sleepwalking or a portion of their brain is essentially still asleep because of that leaky thalamus. So, it is trying to make sense of it. Your brain was all Your brain will always try to make sense of something. It will always try to process something. So, if it's missing information, it's going to just make up its own, right? It's just going to make up its own, which is exactly where the hallucinations come into play. So, whereas they're focused on the hippocampus, they're scratching the surface, whereas though they need to be focusing on the thalamus within, okay? And a little sidebar for y'all.
All right. Anybody who is on a low-carb diet, just know that you are slowly killing yourself because your brain is compiled of mostly carbs. You need to feed yourself carbs in order to keep your brain alive. So, be less focused on the body image, be more concerned about your brain because when I tell you this, your physical health does not take precedent over your mental health. This is a scientific fact. And you can even play into the the placebo effect into this. Mind over matter. Your brain will always come first. Your brain sees your body as a shell, right? So, if you were to become asphyxiated, or if you were to be in a fire of some sort, your brain is going to tell you to shut down. It's going to make you pass out because it is trying to save itself. It does not care about the body. So, the brain should always come first. So, if you're on a low-carb diet, you are increasing your chances of developing dementia. If you are not regulating your glucose, not only are you going to, you know, develop diabetes, but you are also inhibiting your thalamus, which means you are more likely to develop um uh Alzheimer's.
Anyway, getting back to schizophrenia.
So, basically, what I'm arguing, and this is what I wrote down for my paper, schizophrenia is fundamentally a disorder of the thalamic filter, where a breakdown in the BBB, the blood-brain barrier, and the um glutamatergic gluta Yeah. Uh signaling causes a leaky relay system leading to sensory overload and hallucinations um characteristic of the disease itself. Because when you look at MRIs within these patients, they often have a higher permeability in the thalamus. The TRN is failing to kind of like suppress the noise, which is leading to the positive symptoms, which would be like hallucinations. The glutamic connection, if it's dysregulated, um then the signals prevent the filter from closing, which means that it's going to cause, you know, help cause that hallucinations.
The brain is going to try and connect it itself. I'm just really excited about this because I feel like the thalamus is being neglected, and if you ask the right questions, if you go a little bit deeper, you actually see leaky thalamus with those patients who actually suffer from ADD. ADD patients also have a leaky valve. And a lot of people are like, well, what can cause a leaky valve? A lot of stuff can cause your your thalamus to become leaky. You're talking a brain injury, seizure, stroke. I mean, the list goes on. Even some people even argue that ADD can cause a leaky valve.
When actually, I think it is the opposite. A leaky valve is one of the core causes of ADD. I don't understand why are we not focusing on the the first the like literally the circuit board of the brain. It doesn't make sense to me and I'm really excited about this because if I am able to present it to the right people, if I am able to give it over to Yale or the Mayo Clinic or any like WashU Medicine or anything else like that, maybe they can take this information and they can start studying and take it a little bit further and we can actually help schizophrenic patients. I really wish that I could have a control group and a group that I focus on their glucose levels and their glutamate and I I want to see how their symptoms react in both um what we're used to and this new theory. Right?
Because the theories that they're doing right now make no [ __ ] sense whatsoever. Are you telling me that you think the hippocampus is responsible for you having hallucinations?
That makes no [ __ ] sense. Thalamus communicates to the hippocampus. It communicates the amygdala. It has all these neurons inside of it that literally give out where it you know, the communication is supposed to go.
There's a lot of deeper information that I can go into like um the mGluRs or mGluRs like I like to say whenever I'm alone, but um I can go into like the the the TRN and everything else like that, but it's it's there's a lot more information that I can give on it, but basically that is the synopsis. That is the overall view of it is it's the [ __ ] thalamus. And the thalamus is being neglected, which means we are not fixing the problem. We are applying a band-aid.
Now again, it could be because Big Pharma, you know, they don't want to fund it because, you know, sick people make more money than healthy people. You know what I mean? I don't know the reason why I, you know, it's taking them this long, but this is huge. And I I I'm I don't even know what to say.
I'm going to push this out and research it as much as I possibly
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