😵‍💫 Skitzocow Stephen William Lafleur / henstepl / Thisismyrofl / Elecbullet - Schizophrenic Arsonist Who Hates Soda

Just saying hi for when this thread is used as evidence in a court of law.
I honestly wonder if he told his public defender that he went online and skitzo posted all over the website he made the arson threat on. I'm sure that guy is going to have a wonderful day when this case lands on his desk or he finds out about the mountain of evidence archived on an internet autism forum.
 
Has this guy figured out that being disgusted by carbonated drinks is a common side effect of Topamax yet?
I'm not on Topamax. Topamax was what got me investigating the potential for carbonation grimace as an in-born indicator of the brain. Now I've interviewed a number of people who have it, and they're all immune to headaches, and a good portion of them have otherwise-unexplained coprolalia. There's a link.
 
I do agree that medications can, and do, alter the mechanisms of the brain, usually for the worse. But I am not sure if it is as clear-cut as you might think that it is; one medication can result in a wide variety of symptoms in many people, akin to multi-finality.
 
I do agree that medications can, and do, alter the mechanisms of the brain, usually for the worse. But I am not sure if it is as clear-cut as you might think that it is; one medication can result in a wide variety of symptoms in many people, akin to multi-finality.
Though there's a relation between inborn carbonation grimace and severe symptoms as I describe, the relation between Topamax and soda is obfuscated by its carbonic anhydrase inhibition. That's an aversion to soda in its own right. Still, if the drug depletes glutamate through the precise mechanism I propose, which is consistent with the data from this study, the drug could cause two aversions to soda. And then - "whatever Topamax does, you'll have been born with."

Let me be the first to say that glutamate hypofunction can obviously present in many ways. It's the most abundant neurotransmitter in the nervous system, and I argue it has tremendous and complicated consequences in deficiency. And the deficiency is not trivial to resolve: three reasons are fatigue from glutamate/GABA conversion, risk of cell death through excitotoxicity, and incapacitating "transitional voids" between the G-states I've described. Doctors don't know or care to learn these things, and then you end up teaching them.

Yes, I could teach a whole lecture about what the syndrome means, I could bore anyone that isn't a sufferer. But that being the case, and so too that glutamate is the neurotransmitter doctors decline to discuss, I might as well have named the hypofunction after myself, no?
 
Well, even if you might be wrong about some of it, it is at least interesting to hear about. I knew a girl several years ago online who didn't develop that symptom despite taking Topamax, which we both thought was odd, although she did admit that it inhibited her thought processes. Supposedly the medication renders you as dumb as a bag of rocks, although I am not sure if the effects are permanent.
 
Though there's a relation between inborn carbonation grimace and severe symptoms as I describe, the relation between Topamax and soda is obfuscated by its carbonic anhydrase inhibition. That's an aversion to soda in its own right. Still, if the drug depletes glutamate through the precise mechanism I propose, which is consistent with the data from this study, the drug could cause two aversions to soda. And then - "whatever Topamax does, you'll have been born with."

Let me be the first to say that glutamate hypofunction can obviously present in many ways. It's the most abundant neurotransmitter in the nervous system, and I argue it has tremendous and complicated consequences in deficiency. And the deficiency is not trivial to resolve: three reasons are fatigue from glutamate/GABA conversion, risk of cell death through excitotoxicity, and incapacitating "transitional voids" between the G-states I've described. Doctors don't know or care to learn these things, and then you end up teaching them.

Yes, I could teach a whole lecture about what the syndrome means, I could bore anyone that isn't a sufferer. But that being the case, and so too that glutamate is the neurotransmitter doctors decline to discuss, I might as well have named the hypofunction after myself, no?
I read what you gave us, and, while I didn't understand most of it, it made me very sad. I totally get the concept of paying someone a lot of money to point me to someone else, and on and on. Finally I just figured it out for myself.

Best wishes.
 
Though there's a relation between inborn carbonation grimace and severe symptoms as I describe, the relation between Topamax and soda is obfuscated by its carbonic anhydrase inhibition. That's an aversion to soda in its own right. Still, if the drug depletes glutamate through the precise mechanism I propose, which is consistent with the data from this study, the drug could cause two aversions to soda. And then - "whatever Topamax does, you'll have been born with."

Let me be the first to say that glutamate hypofunction can obviously present in many ways. It's the most abundant neurotransmitter in the nervous system, and I argue it has tremendous and complicated consequences in deficiency. And the deficiency is not trivial to resolve: three reasons are fatigue from glutamate/GABA conversion, risk of cell death through excitotoxicity, and incapacitating "transitional voids" between the G-states I've described. Doctors don't know or care to learn these things, and then you end up teaching them.

Yes, I could teach a whole lecture about what the syndrome means, I could bore anyone that isn't a sufferer. But that being the case, and so too that glutamate is the neurotransmitter doctors decline to discuss, I might as well have named the hypofunction after myself, no?

Is there any medication or treatment for carbonation grimace?
 
Also, the excess glutamate in their brains overstimulates the dopaminergic neurons,
If a neuron is dopaminergic, that means it has receptors for dopamine, not glutamate, not any other neurochemical. While it is true that a single neuron can release multiple transmitters from different types of synapses, they generally only have one type of receptor. As for your theories about autism being caused by gut microbes, that's a Dan Ciley woo-tier take I won't even touch on..

@henstepl
In all due respect, your notions of how neuromodulators/neurotransmitters affect the brain are incredibly binary, oversimplistic and just generally wrong. I gave you some credit for refuting the monoamine theories of schizophrenia and depression, but then you went ahead and exchanged one arbitrarily categorical theory for another.
There are dozens of different types of receptor proteins throughout the CNS for each neurotransmitter and, for almost all of them, their effect can in fact be reversed depending on the receptor site the molecule binds to. Dopamine, for example, can depress the brain when bound to D2-4 receptors, but excite activity when bound to D1/5, put very simply. And the duration and propinquity of those effects vary too depending on location and receptor type. Also note that the affects of drugs can influence the transcription factors and change the structural and functional properties of neurons + their networks over time. Overabundance of one particular neuromodulator is not going to radically change your personality from one discrete category into another. In-fact, the fixation on fitting things into types rather than continuous traits is archaic and has for so long been the cause of stagnation in psychology & cognitive neuroscience.
I truly feel you should go and do more thorough research on neurobiology rather than looking for confirming evidence for your existing, steadfast belief in your theory (more like faith). The more I read your posts, the less it appears that you actually have a grasp of what you're talking about; it's dogmatic and lacks unbiased scientific objectivity. Please get professional help, trust your doctor.
 
Última edición:
Is there any medication or treatment for carbonation grimace?
Carbonation grimace either will or won't be reversed itself by facial exercises. I can restore my ability to drink soda, quite often, with a simple duckface. When I can, that's information on top of the grimace itself.

The glutamate hypofunction which carbonation grimace proves can be treated like a glutamate deficiency, but there are certain issues. You mustn't create GABA fatigue (which glutamate will do), you must be careful not to cause cell death (which leads me to use serine), and I argue that there are transitional voids between G-states which are uncomfortable and disorienting, to be traversed sparingly.
 
Excellent contender for random.txt. Also, this is apparently the archetypal hot woman for our resident soda-hater.
Ver archivo adjunto 1796691

Vapid instathot, who became famous literally because BOOBS and now considers herself a paragon of feminism. Also, I suggest that you look up the interview she gave recently to some glossy trashrag where she decries how horrified she was that she's going to bring yet "another white male" into the world.

Namely, you have no education in chemistry, biological or food

He does have a broken brain but just to be sure, lack of formalized education, in theory, doesn't mean that conclusions he might come to would be inherently incorrect. In the age when purported scientists have sold their credibility for a chance to be used as political puppets, your advanced degree means jack shit.
 
Última edición:
If a neuron is dopaminergic, that means it has receptors for dopamine, not glutamate, not any other neurochemical. While it is true that a single neuron can release multiple transmitters from different types of synapses, they generally only have one type of receptor. As for your theories about autism being caused by gut microbes, that's a Dan Ciley woo-tier take I won't even touch on..

@henstepl
In all due respect, your notions of how neuromodulators/neurotransmitters affect the brain are incredibly binary, oversimplistic and just generally wrong. I gave you some credit for refuting the monoamine theories of schizophrenia and depression, but then you went ahead and exchanged one arbitrarily categorical theory for another.
There are dozens of different types of receptor proteins throughout the CNS for each neurotransmitter and, for almost all of them, their effect can in fact be reversed depending on the receptor site the molecule binds to. Dopamine, for example, can depress the brain when bound to D2-4 receptors, but excite activity when bound to D1/5, put very simply. And the duration and propinquity of those effects vary too depending on location and receptor type. Also note that the affects of drugs can influence the transcription factors and change the structural and functional properties of neurons + their networks over time. Overabundance of one particular neuromodulator is not going to radically change your personality from one discrete category into another. In-fact, the fixation on fitting things into types rather than continuous traits is archaic and has for so long been the cause of stagnation in psychology & cognitive neuroscience.
I truly feel you should go and do more thorough research on neurobiology rather than looking for confirming evidence for your existing, steadfast belief in your theory (more like faith). The more I read your posts, the less it appears that you actually have a grasp of what you're talking about; it's dogmatic and lacks unbiased scientific objectivity. Please get professional help, trust your doctor.
Remember I haven't received an actual diagnostic effort, but I suppose you could chalk that up to my always beginning with my own narration. When you direct me to trust my doctor, you're exposing us both to the haughty risk that he'll tell me that his summary observation is of no mental disorder at all. These things are subtle until they aren't, and I know from experience that I have too much to lose and too many voids to pass through to trust him to that extent, from that brief observation.

And remember that glutamate is the neurotransmitter that doctors will bill you money to decline to discuss.

Let me say that I hear you when you say I've simplified, and I'll simplify a bit more by chopping it down to the adrenaline+serotonin-dopamine-choline=psychopathy theory, because I figure I've had a number that you've objected to, and we need something to focus on. I've based that prediction off of the plausible serotonin bursts I have every night, and off of the hangover state. When I transition into psychopathy, it's not a sudden affective flip. It is PRECEDED and SUCCEEDED by an incapacitating zero-intelligence void. When I compare the middle to what comes before and after this exhausting process, I can only conclude the differences I notice point to something, rather than nothing.

Let me ask you this: you can take a very neurotypical brain with all four transmitters, and you can subtract choline and dopamine through ways and means. When it's 70/30 for the chemicals I describe, do you care to issue, from an educated stance, any predictions about the adrenaline-serotonin brain? Or should my claims be weighed against - no claims at all?
 
Remember I haven't received an actual diagnostic effort, but I suppose you could chalk that up to my always beginning with my own narration. When you direct me to trust my doctor, you're exposing us both to the haughty risk that he'll tell me that his summary observation is of no mental disorder at all.

may i ask, do you mean here that you disagree with the many diagnoses you have received? and as a follow-up, that you would now receive no diagnosis if examined by a traditionally educated psychiatrist? i recognize your investment in defining and researching florian syndrome but in the interim how do you expect the medical and psychiatric community to be of help to people such as yourself?
 
Let me ask you this: you can take a very neurotypical brain with all four transmitters, and you can subtract choline and dopamine through ways and means.
I can't even begin to have a discussion with you because the things you suggest do not make any kind of sense and you're just throwing around empty words and unfounded 'hypotheses', or hunches, about how the brain works. I don't have predictions about the 'adrenaline-serotonin' brain because the idea of an entire human body and mind being driven solely by 4 separately weighted forces is just an unhelpful and meaningless assumption. That's the point of what I'm saying, there's nothing to be gained in a discussion when your convictions are based on non-facts. My answer would mean as little toward the pursuit of knowledge as a speculation on whether the spaghetti monster is Bolognese or carbonara. (Incidentally, what about GABA, Glutamate and noradrenaline (AKA norepinephrine)? Choline isn't a neurotransmitter by the way, it's acetylcholine.)
Refer back to the bit where i said the effect of a given neuromodulator may be reversed depending on where it binds, meaning that there's no straightforward 'serotonin' effect.
 
Última edición:
I can't even begin to have a discussion with you because the things you suggest do not make any kind of sense and you're just throwing around empty words and unfounded 'hypotheses', or hunches, about how the brain works. I don't have predictions about the 'adrenaline-serotonin' brain because the idea of an entire human body and mind being driven solely by 4 separately weighted forces is just an unhelpful and meaningless assumption. That's the point of what I'm saying, there's nothing to be gained in a discussion when your convictions are based on non-facts. My answer would mean as little toward the pursuit of knowledge as a speculation on whether the spaghetti monster is Bolognese or carbonara. (Incidentally, what about GABA, Glutamate and noradrenaline (AKA norepinephrine)? Choline isn't a neurotransmitter by the way, it's acetylcholine.)
Refer back to the bit where i said the effect of a given neuromodulator may be reversed depending on where it binds, meaning that there's no straightforward 'serotonin' effect.
Sure, I'm lazy enough to refer to noradrenaline as adrenaline, and acetylcholine as choline - nobody wants to say "acetyl", and I don't want to refer to two neurotransmitters starting with "A". I can't tell you much about GABA except it makes me tired, but Glutamate is the one that's deficient in my brain, and the biggest (hypo)theses I write are elucidations of what that deficiency does. It's fitting you should ask, because what's on the books frankly doesn't inform on shit compared to what I've learned about that deficiency, and I've learned more than I could ever bother you with.

And you wouldn't have anything to say about glutamate deficiency, either, because you declined to describe the adrenaline-serotonin brain, when everyone else who's watching the thread knows that I'm aware enough of more reduction ways-and-means than you, and I regularly achieve that brain. Don't get so lost in the receptors you and I both know: there is a straightforward serotonin effect - and serotonin can be straightforwardly affected, through SSRIs or tianeptine...

... and the serotonin affect is the upper half of the face. This is why SSRIs cause me to have carbonation grimace.

may i ask, do you mean here that you disagree with the many diagnoses you have received? and as a follow-up, that you would now receive no diagnosis if examined by a traditionally educated psychiatrist? i recognize your investment in defining and researching florian syndrome but in the interim how do you expect the medical and psychiatric community to be of help to people such as yourself?
Someone said it was sad to be pointed from one doctor to another, but what's worse is for a doctor to point you nowhere, leave you no better than you started, and bill you. I don't know how psychiatrists are comfortable leaving my psychiatry incomplete, but they do.

Everything I've received is either a half-assery nobody believes ("psychotic disorder" is what rich kids get told when their parents lock them in hospitals so they don't go to jail) or incomplete at best (Tourette syndrome, when I don't even match it). If anybody had the balls to approach me about carbonation grimace and assert it's a delusion, and set themself up for the possibility that it's not, that'd be the only way I'd get a schizophrenia diagnosis. Because to have schizophrenia you need delusions or hallucinations, and I haven't got them.
 
Atrás
Top Abajo