Great post, I'll read the actual article when my head is in a better shape.
I always say that I'll go back on Haldol if I end up in a terrible state and just can't manage without. I really hope that my brain has, like, rebooted by now, after six years off meds. I really hope that if I try Haldol again it will work as well as it initially did. Before it lost most of the desired effect, and instead began producing some really nasty side effects.
But as of now, I'm trudging along, even though I'm currently a little fucked up (probably overworked, end of semester and all that). Monday morning I looked in the mirror and my face was completely skewed, lopsided like a Picasso painting. My first instinct was to try to paint it into a straighter shape with make-up, but then I thought no, I'm gonna go about this rationally. I'm gonna double-check what my face looks like on other devices. So I checked my phone on mirror mode, and started a one-person Zoom meeting on the computer, and my face looked normal in both. Then I thought ok, it's just a mirror illusion. But I need to cancel some shit and calm down.
Now I've cancelled some shit and try to take it really easy. Hanging in there.
Great post! I'll share it with a PGY-3 resident I’m advising.
Here’s a related question: When I trained, we were taught that “as-needed” antipsychotic treatment—that is, stopping the medication after resolution of an acute exacerbation and restarting only after a relapse—was not advisable compared to continuous antipsychotic treatment.
Over time, long-acting injectables (LAIs) have been increasingly promoted as being more effective at preventing relapse. But this raises another question: what about intermittent dosing? Not “as-needed,” but regular, yet intermittent dosing. For example, there’s been some suggestion that strategies like taking Zyprexa 10 mg every three days might be “good enough.”
Why consider this kind of intermittent dosing? The rationale - theoretical? realistic? - was a concern about long-term adverse effects such as supersensitivity psychosis, tardive dysmentia, chronic up-regulation of dopamine receptors, and of course, tardive dyskinesia. The idea was that allowing the brain to “reset” between doses might theoretically reduce the risks associated with continuous exposure to the medication.
However, the introduction of LAIs—presumably superior at preventing relapse—ensures an even steadier and more consistent exposure to the medication.
I bring up this question not knowing whether there will ever be enough funding or interest to research this approach, but I’d love to hear thoughts on it!
There is something about decreased oxygenation that is not being studied by mainstream psychiatry and also not controlled for in comparison studies. It would explain why individuals with schizophrenia complain of head numbness, light headedness, dizziness, and various somatic issues, regardless of medication naivety or dose.
Whether its from chain smoking (as is widely known in schizophrenia), repeat binge drinking (ubiquitous), lack of aerobic exercise whatsoever (e.g. merely walking, not running), associations between proclivity toward ANY altered state of consciousness versus mild sleep apnea (highly underdiagnosed in <40 year olds), high fructose/glucose diets (decreases oxygenation), or poor sleep regimens in general (also decreases global oxygenation) and so on, no one in psychiatry wants to study these. Because decreased oxygenation is not as sexy sounding as the "big-bad-broken gene polymorphism" to the genetcists, or the "big bad broken dopamine receptor" to the chemists, or the big bad broken neural networ to the MRI crowd, or the big bad broken belief system that the cognitivists want to talk about, and so on.
I believe these de-oxygenating factors collectively contribute to the negative symptoms side, but NOT directly toward the positive symptoms side. Rather, it is when the negative symptoms become so severe, that one intentionally pushes themselves toward altered states (positive symptoms), because it is positive symptoms that makes one feel alive again when negative symptoms becomes dissuptive. Then they get addicted to those same altered states (positive symptoms), because they make one feel too alive, God-like perhaps, and then we surpass a critical threshold, and we get psychosis. Its not a new idea. Nor is it complex.
If the standard mantra of reductive physicalism is that "More metabolic brain activity automatically means more phenomenal consciousness", and that psychosis means "Too much metabolic activity somewhere in the brain or as a whole", then it automatically implies that anti-psychotic drugs necessarily decrease metabolic activity in particular brain regions or as a whole. Which therefore means de-oxygenation. To deviate from this hypothesis means to question physicalism itself, because then you would be admitting that metabolic activity is either anti-correlated or uncorrelated to brain activity and/or phenomenal consciousness, which then collapses physicalism. I don't know of any mainstream psychiatrists who'd dare to question physicalism, but if they're all so absolutely sure of it, then they'd enthusiastically try to falsify the article above by Turkheimer et al out of spite. Because if you follow Turkheimer's end conclusion, it is indirectly implying something other-than bottom-up physicalism.
Of course for this to work, the "entity realists" or "disorder realists" need to stop postulating mental disorders AS discrete particles or substances that literally occupy space and time, or have mass, charge, or spin, and "act" or have "agentic powers" or are have "causal properties" as in symptoms. Because what the entity realists are really doing here is postulating something over and above the brain or body. They're suggesting TWO separate things: 1). an "entity" called "mental disorder" that is 2). "inside of the brain" rather than starting with and ending with the brain's organization or dynamics. Again, they speak of brains (1 is fine), but then, they speak of mental disorders (2 is the error). The problem cannot be averted by rejecting dualism in passing, because when you postulate a new category "with causal powers" (#2 above), you have just caused everyone to go down the rabbit hole of abstraction "of mental disorders" rather than discussing what brains or bodies do.
Great post, I'll read the actual article when my head is in a better shape.
I always say that I'll go back on Haldol if I end up in a terrible state and just can't manage without. I really hope that my brain has, like, rebooted by now, after six years off meds. I really hope that if I try Haldol again it will work as well as it initially did. Before it lost most of the desired effect, and instead began producing some really nasty side effects.
But as of now, I'm trudging along, even though I'm currently a little fucked up (probably overworked, end of semester and all that). Monday morning I looked in the mirror and my face was completely skewed, lopsided like a Picasso painting. My first instinct was to try to paint it into a straighter shape with make-up, but then I thought no, I'm gonna go about this rationally. I'm gonna double-check what my face looks like on other devices. So I checked my phone on mirror mode, and started a one-person Zoom meeting on the computer, and my face looked normal in both. Then I thought ok, it's just a mirror illusion. But I need to cancel some shit and calm down.
Now I've cancelled some shit and try to take it really easy. Hanging in there.
I hope this has influence.
Great post! I'll share it with a PGY-3 resident I’m advising.
Here’s a related question: When I trained, we were taught that “as-needed” antipsychotic treatment—that is, stopping the medication after resolution of an acute exacerbation and restarting only after a relapse—was not advisable compared to continuous antipsychotic treatment.
Over time, long-acting injectables (LAIs) have been increasingly promoted as being more effective at preventing relapse. But this raises another question: what about intermittent dosing? Not “as-needed,” but regular, yet intermittent dosing. For example, there’s been some suggestion that strategies like taking Zyprexa 10 mg every three days might be “good enough.”
Why consider this kind of intermittent dosing? The rationale - theoretical? realistic? - was a concern about long-term adverse effects such as supersensitivity psychosis, tardive dysmentia, chronic up-regulation of dopamine receptors, and of course, tardive dyskinesia. The idea was that allowing the brain to “reset” between doses might theoretically reduce the risks associated with continuous exposure to the medication.
However, the introduction of LAIs—presumably superior at preventing relapse—ensures an even steadier and more consistent exposure to the medication.
I bring up this question not knowing whether there will ever be enough funding or interest to research this approach, but I’d love to hear thoughts on it!
There is something about decreased oxygenation that is not being studied by mainstream psychiatry and also not controlled for in comparison studies. It would explain why individuals with schizophrenia complain of head numbness, light headedness, dizziness, and various somatic issues, regardless of medication naivety or dose.
Whether its from chain smoking (as is widely known in schizophrenia), repeat binge drinking (ubiquitous), lack of aerobic exercise whatsoever (e.g. merely walking, not running), associations between proclivity toward ANY altered state of consciousness versus mild sleep apnea (highly underdiagnosed in <40 year olds), high fructose/glucose diets (decreases oxygenation), or poor sleep regimens in general (also decreases global oxygenation) and so on, no one in psychiatry wants to study these. Because decreased oxygenation is not as sexy sounding as the "big-bad-broken gene polymorphism" to the genetcists, or the "big bad broken dopamine receptor" to the chemists, or the big bad broken neural networ to the MRI crowd, or the big bad broken belief system that the cognitivists want to talk about, and so on.
I believe these de-oxygenating factors collectively contribute to the negative symptoms side, but NOT directly toward the positive symptoms side. Rather, it is when the negative symptoms become so severe, that one intentionally pushes themselves toward altered states (positive symptoms), because it is positive symptoms that makes one feel alive again when negative symptoms becomes dissuptive. Then they get addicted to those same altered states (positive symptoms), because they make one feel too alive, God-like perhaps, and then we surpass a critical threshold, and we get psychosis. Its not a new idea. Nor is it complex.
But to your article - perhaps you could see https://academic.oup.com/schizophreniabulletin/article/46/3/484/5637929 .
If the standard mantra of reductive physicalism is that "More metabolic brain activity automatically means more phenomenal consciousness", and that psychosis means "Too much metabolic activity somewhere in the brain or as a whole", then it automatically implies that anti-psychotic drugs necessarily decrease metabolic activity in particular brain regions or as a whole. Which therefore means de-oxygenation. To deviate from this hypothesis means to question physicalism itself, because then you would be admitting that metabolic activity is either anti-correlated or uncorrelated to brain activity and/or phenomenal consciousness, which then collapses physicalism. I don't know of any mainstream psychiatrists who'd dare to question physicalism, but if they're all so absolutely sure of it, then they'd enthusiastically try to falsify the article above by Turkheimer et al out of spite. Because if you follow Turkheimer's end conclusion, it is indirectly implying something other-than bottom-up physicalism.
Of course for this to work, the "entity realists" or "disorder realists" need to stop postulating mental disorders AS discrete particles or substances that literally occupy space and time, or have mass, charge, or spin, and "act" or have "agentic powers" or are have "causal properties" as in symptoms. Because what the entity realists are really doing here is postulating something over and above the brain or body. They're suggesting TWO separate things: 1). an "entity" called "mental disorder" that is 2). "inside of the brain" rather than starting with and ending with the brain's organization or dynamics. Again, they speak of brains (1 is fine), but then, they speak of mental disorders (2 is the error). The problem cannot be averted by rejecting dualism in passing, because when you postulate a new category "with causal powers" (#2 above), you have just caused everyone to go down the rabbit hole of abstraction "of mental disorders" rather than discussing what brains or bodies do.
Your work is so refreshing, and I appreciate how you make it accessible to those not in the clinical research space. I hope more people see this!