Question: Hi,

I received a diagnosis three years ago after a psychiatric hospital stay. However, I have strong reason to believe that this diagnosis is false.

I shall attach my full story and analysis of this. At the bottom are questions for review.

Given the evidence and circumstances in the story shared (which will be attached in a document), do you find enough reason to believe that the diagnosis given was in fact, misgiven?

Hi,

I received a diagnosis three years ago after a psychiatric hospital stay. However, I have strong reason to believe that this diagnosis is false.

I shall attach my full story and analysis of this. At the bottom are questions for review.

Given the evidence and circumstances in the story shared (which will be attached in a document), do you find enough reason to believe that the diagnosis given was in fact, misgiven?

Email shall be forthcoming soon. Thank you

Email shall be forthcoming soon. Thank you

ATTN: Dr Seikhoo Bishnoi (Psychiatrist)

Attachment enclosed.

ATTN: Dr Seikhoo Bishnoi (Psychiatrist)

Attachment enclosed.

I apologize for the formatting, I have copied and pasted the text, nd it has come up in this manner.

Thank you for your time.

"NYU - APRIL 2016

During the spring of 2016, I was planning to try a particularly pure and well-reputed version of a little-known Soviet-created “smart drug,” an anxiolytic substance that I had dabbled with before in the past in a recreational manner—a substance known as Phenibut.

As an “over the counter,” non-regulated pro-GABA drug, it acts similarly to alcohol or to benzodiazepines, except without as strong of a factor of sedation.

The Phenibut drug had seen an increase in recreational use in recent years by this time. While it was known to be particularly effective at making social events and parties more enjoyable, some online communities had began discussing the potential concurrent use of a second type of nootropic or smart drug known as Fasoracetam. This drug is believed to work in some kind of synergistic manner to Phenibut, as some people reported that it seems to reduce the negative after-effects of Phenibut use.

To note: As these are two drugs both relatively unknown to Western pharmacology, with on of them being Soviet-invented and the other having been invented relatively recently, there were absolutely no case studies or reported information in the medical literature on what happens when anyone combines these two in amounts.

What were the dosage standards? Brand name Russian Phenibut, which is called (R)-Phenibut (being the only psychoactive enantiomer compared to racemic (R,S)-Phenibut), is recommended up to XXXXXXX dose of 2,250mg daily. Extrapolating this dose to racemic Phenibut, which was the version I possessed, this would logically double to 4,450 mg XXXXXXX dose per day, as this amount of racemic Phenibut contains 2,250 mg of the psychoactive portion, which is the (R)-enantiomer of the drug.

Recreational doses, according to many sources online, go northwards from 2 -3 grams per day, and often reach as high as 7 - 10 grams per day with some users. I decided I would definitely stay below the 7 - 10 gram range, as this is close to double the recommended XXXXXXX dose that is intended for daily use.

With Fasoracetam, the recommended dosages, according to most sources and literature available at the time, seemed. to be more flexible, and ultimately less restrictive. Various sources showed a large range of dosage, ranging from 100 mg per day, to upwards of 800 mg per day, to be safe for dosage. I decided I would not consume more than “roughly a few hundred milligrams” of this second substance per day as well.

According to all material available to me at the time, there were no indications to show that users taking Phenibut recreationally experienced any significant danger or damage. The same applied to Fasoracetam, which was considered to be largely much more safe in comparison as well. Additionally, there were limited anecdotal reports available by users who had indicated that they use the mixture of the two drug with no problem or adverse effects to report.

Therefore, I decided I would conduct a limited testing of these drugs over a three-day period, during which I consumed on each day (or each evening, with daily doses broken down and taken over the course of several hours): approximately a few grams of Phenibut each evening, along with a few hundred milligrams of Fasoracetam.

After the first two days of use, no ill reports or side effects were noted. While I presumed to conclude that this meant that these I decided I would dose for one additional evening on the third day using only slightly higher amounts than those used on the first two days, before planning to take a few days of break to allow these drugs to cycle out of my system and report findings to the online nootropic (smart drug) community.

However, after by the end of the third evening, I lost consciousness—and ended up in a coma at a local hospital by morning.

…

**********
“Phenibut Overdose in Combination with Fasoracetam: Emerging Drugs of Abuse - jcicm-aid1001.pdf”
https://www.heighpubs.org/jcicm/pdf/jcicm-aid1001.pdf
**********

My story, according to the relevant research departments at this hospital:


INTRODUCTION

“The widespread availability of non-traditional dietary supplements and pharmacologically active substances via the Internet continues to introduce mechanisms for inadvertent toxidromes not commonly seen. Consumers are virtually unrestricted in their ability to acquire products purporting augmentation of normal physiology for the purposes of enhancement, recreation, and/or potential abuse. The safety profiles at standard or toxic doses remain largely unknown for many agents that can be purchased electronically. We report a case of mixed toxicity related to phenibut and fosaracetam, both of which are readily available for consumer purchase from online retailers. Written and verbal consent was obtained for this case presentation.

CASE REPORT 

“A 27-year-old male with a past medical history of anxiety was discovered unresponsive on the sidewalk. Paramedics responding to the scene noted that the patient had an initial Glascow Coma Score (GCS) of 3 and possessed an empty 5 gram bottle of fasoracetam. During transport to our institution, there were brief periods of severe agitation with emesis. On arrival to our emergency department (ED), the patient exhibited intermittent episodes of agitation and disorientation only upon physical stimulation. Physical exam revealed unremarkable respiratory, abdominal, and musculoskeletal systems. Notably, there were no abnormal pupillary changes or clonus. His vital signs were characterized by normal blood pressure of 135/62 mm Hg, respiratory rate of 12 breaths/min, and an oxygen saturation of 95% on room air. The most signiβicant βinding was a sinus bradycardia with a heart rate of 36 beats/min, for which the patient received 0.5 mg atropine sulfate resulting in a short-lived response to 70 beats/min. All laboratory measurements were within normal limits. Levels for acetaminophen, digoxin, salicylate, and ethanol were not detected. Bedside urine toxicology immunoassay was negative for benzodiazepines, tricyclic antidepressants, cocaine, amphetamines, tetrahydrocannabinol, opioids, barbiturates, phencyclidine and ketamine. A non-contrast CT head ruled out any contributing intracranial pathology.

“While in the ED, the patient remained somnolent, and persistently bradycardic with heart rates ranging from 34 to 50 beats/min requiring placement of transcutaneous pacing pads. The patient displayed amnesia to all events preceding his presentation. He acknowledged that his current state deviated from his normal baseline neurologic and functional status. The patient denied any recent illicit, prescription, or over-the counter drug use, reported social alcohol consumption, and recent use of fasoracetam to enhance mental capacitance and alertness.

“After 24 hours, the patient was able to recall that he purchased phenibut 99.5% powder 100 grams, and fasoracetam powder 5 grams through LiftMode and Nootropics Depot with the intention to stabilize his ‘GABA system’. Two days prior to admission, he was taking phenibut 500mg three times a day and fasoracetam 50-100mg daily. On presentation, he reported that he went to a party and took 10 grams of phenibut and an unknown amount of fasoracetam. On hospital day 2, his lethargy and bradycardia was mostly resolved but complained about increasing anxiety, hallucinations, and delusions of grandeur. He was evaluated by the psychiatric team, and was admitted to the psychiatric unit for evaluation and management of his underlying psychosis. 

DISCUSSION

“Racemic phenibut is a GABAB agonist that possesses anxiolytic and nootropic activity mainly attributed to its R-enantiomer [1]. It is structurally similar to baclofen but differs by the presence of one chlorine atom in the benzene ring and is 30 times less active as a GABAB agonist [2]. Other pharmacological activity includes decreasing the activity of voltage-dependent Ca2+ ionic channels similarly to gabapentin and possibly GABAA agonism at high doses [1,2]. Limited information is available on the pharmacokinetics of phenibut. After systemic absorption, phenibut is rapidly distributed to the brain, kidneys, liver, and urine. The elimination half life is 5.3 hours and 65% of the parent drug is excreted into the urine [1,2].

“All published acute toxicities from phenibut are summarized in Table 1 [3-9]. Oral administration of phenibut was the most common route with doses ranging from 1 gram to 30 grams with single oral administration. The onset of desired effects was reported to occur within 2-4 hours following oral ingestion with an overall duration of 7-24 hours. Most patients presented with altered mental status, low levels of consciousness, and agitation upon arousal. In cases characterized by severe agitation, benzodiazepines and antipsychotics demonstrated minimal to moderate effects. All patients were carefully monitored in either an emergency observation or intensive care unit and most were discharged within 24-48 hours from admission.

“In contrast to previously reported cases, our patient was also taking fasoracetam which stimulates metabotropic glutamate receptors, up-regulates GABAB receptors, and stimulates the release of acetylcholine from central cholinergic neurons [10]. It is absorbed rapidly after oral administration and has a bioavailability of 79%-97%. The elimination half-life ranges from 4-6.5 hours and is predominately excreted in the urine as unchanged drug [10]. Fasoracetam (NFC-1) has recently obtained an Investigational New Drug (IND) from the Food and Drug Administration to be evaluated in patients with ADHD who have rare glutamate gene mutation and has a well-established safety profile from previous clinical trials at recommended doses (50-800mg a day in divided doses) [10]. The most commonly reported side effects include headache and fatigue. Nevertheless, large doses of fasoracetam could potentially explain the bradycardia experienced by this patient as it is not seen with the reported cases of phenibut overdoses. In addition, fasoracetam could potentially enhance the response to phenibut through the up-regulation of GABAB receptors and decrease the threshold for tolerance that is commonly observed with phenibut.

“Phenibut and fasoracetam are widely available from internet sites that are mainly based in the UK and USA [2,8]. These unregulated products place the general public at risk from overdoses and can produce unique toxidromes especially with co-administration of multiple supplements. The clinical management is primarily supportive, but should incorporate a thorough history of recent medication use, including dietary supplements and vitamins. In the majority of phenibut overdoses, the toxicological properties predominantly effects the central nervous system and to a lesser extent the cardiovascular system. Healthcare providers should be prepared to manage or inform patients about the acute excess or withdrawal side effects after phenibut or fasoracetam overdoses [11].”

…

The article above does a satisfactory job of conveying the gist of what happened. I was found unconscious in public and brought into NYU Hospital in New York, where I remained in a coma for about 12 or so hours. Once I awoke, I proceeded to be observed for a few days in Step-down from ICU unit.

A few things of importance also took place during the first few days, as well as during the subsequent days, that all tie in to a certain body of information, as well as into a narrative regarding an ongoing state of health that I have been dealing with to this day, on the medical aspect. The medical side of the story, and the after-effects that I have been living with, is a side of the story that I discuss much more deeply in a separate set of documents that I have compiled over the last three years. The information presented therein in slightly out of the scope of this document, as I am here to present more of the procedural aspects of what happened, in the context of mis-diagnoses within the psychiatric domain. I encourage the interested reader to read my other documents for more information on what happened in the hospital, as well as ongoing issues stemming from the use of these drugs.

The relevant portions of the story, however, I will describe below.

…

A day or two prior to being discharged from the ER/ICU side of the hospital, I agreed to undergo voluntary admission into the hospital’s psychiatric unit, in order to be observed and to be able to manage any potential withdrawals from these drugs, and to also give the hospital a chance to make sure that I’m fully recovered and stabilized at the psychological level.

Importantly: I have had absolutely no prior medical history of mental illness whatsoever, with no mental diagnosis being made, through up until this time being in the hospital. Moreover, I have been functional through up until this time, with there being no assumption, no suspicion, no evidence and no accusation of mental illness or mental illness symptoms present anywhere in the past or present, in my life.

Moreover, according to all information available on the post-effects of Phenibut and/or Fasoracetam, on the development of mental illness?

There is none whatsoever; all discharges reported in the other related cases summarized above make implication that no further evidence or psychological damage was present at all, as the effects of the drug are transient and largely benign psychologcally—this is with the exception of one particular aspect, that is important to highlight.

When I spoke to the nurses during my ER/ICU stay, they asked me how I felt. When I told them I felt very good, they kind of laughed, and remarked among themselves, saying, “Just wait till the withdrawals start kicking in…”

Another nurse, wishing to tip me off on what would likely be happening, printed out a medical document and showed me something that basically mirrored what the following quote from the Maryland Poison Control Center states:

“Withdrawal symptoms [from Phenibut], which can last two weeks or longer, may include anxiety, agitation, fatigue, hallucinations, … In addition, symptoms for which phenibut was taken will return. Treatment includes supportive care and benzodiazepines for agitation.”

—Hallucinations!! Imagine that.

Most people in general associate hallucinations with two things: legitimate mental disorders, and also hallucinations as part of the positive drug effects given from hallucinogenic drugs like LSD.

However, fewer people understand that, while hallucinogenic drug gives you hallucinations when you’re on them, other types of drugs—notably the GABAergic type, of which Phenibut is one (along with alcohol, bentos and others)—can produce hallucinations and delirium tremens when you are gong OFF of these drugs! This is due to the short-lived exposure of tolerance and down regulated GABA receptors, once drug level begin to lower. It is after a short period of time that these receptors reset back to their default setting only in, and following, the absence of the drug, and the person returns to normal function.

I am glad that this nurse tipped me off, because I had no idea at that time that something like this was possible. Surely enough, the withdrawals, consisting of agitation and hallucinations too, stated to kick in. In addition to these symptoms were symptoms of delusion or false-belief, which go hand-in-hand with GABAergic withdrawal patterns, and is clearly understood by competent professionals to be distinctly limited to the withdrawal phase in otherwise-normal population.

After a few days, and before the withdrawals completely subsided, I had transferred to the psychiatric facility. But before we proceed to discuss how this ended up turning out, I’d like to address the Phenibut + Fasoracetam article mentioned above—as in it, we can see the first instances and causes of what would be a cascading series of mistakes and problems the results of which I would inherit and still be dealing with to this day.

Firstly, to note: We have the subconscious belief, as humans, to take those publications from sources we deem as being authoritative, and consider the information inside as being nothing else other than gospel truth.

Well, after I came across this article months after it was published without my awareness, I was shocked to find at how many pieces of information that they got wrong.

Let us examine.

…

“[The patient] possessed an empty 5-gram [container] of fasoracetam.”

This is true, and in fact gave the ER dept the first large clue that my coma and lack of consciousness was drug-induced—in fact, It was the only clue that they had, as none of their drug tests could uncover the fact that I had multiple such drugs in my system.

However, what was the initial assumption made by the team when they see an unconscious person with an empty drug container? They think I took all of it at once, and that it could have likely been a suicide attempt. (Which isn’t true at all, and I quickly and truthfully refuted this assumption by anyone who posed it.)

“…an unknown amount of Fasoracetam.”

This is a lie. I clearly reported to the doctors and staff the approximate amounts taken, which was within the range I specified, furthermore, this amount was roughly consistent with the amount taken on each of the other two days.

“…a past medical history of anxiety”

This is a complete, bold lie, and it is the most dangerous lie that likely started the problems. After all, I had earlier just explained to the reader, that I have had absolutely no past “medical” history of hardly anything. I also did not make statements about “having anxiety,” which are words that we should be very careful when using, and I shall explain why.

Consider this: what is the difference between sadness and depression? One of them is a normal human emotion that can be experienced regularly—the other is a psychiatric disorder and a mental illness. It is important to note that, of course, only a doctor can diagnose someone with a mental illness. The same goes with any of the others—do you get anxious sometimes, or do you have [the diagnosed mental illness] of anxiety?

An additional quirk of the XXXXXXX system—only a drug (or FDA approved therapy or procedure) can cure or treat illness of any kind, including mental illness, which means that once a mental illness is officially diagnosed, it is “accepted” that it can never legally or medically be “cured”—it can just either “go into remission,” or have it be found that you were “misdiagnosed” in the first place if it is apparent that the illness is not present in a patient.

In fact, making claims that a person “has” any kind of mental illness without it actually being true that the person was factually diagnosed with such an illness? This can cause a person to face court charges for defamation under the law, as our society is very protective of slander and libel, which is what this essentially is.

Keep in mind that at no point during this stay with NYU did anyone ever diagnose me with anxiety. How was this lie of “past medical history of anxiety” constructed for inclusion in an article like this? Allow me to paint the picture: It is as simple as a guy who looks up what Phenibut is generally used for, he finds out that it can “treat anxiety,” and simply goes, “Oh, it must be ‘cause he’s got anxiety!”

A past history of sadness is not the same as a past history of depression. Moreover, a past history of depression is not the same as a past medical history of depression, where n the latter case, as opposed to the former presumably, the supposed depression would be medically documented and diagnosed, and thus legitimately pre-established. Thus, there are multiple layers to the insanity and boldness of this falsity.

Why does this take place? This is subconsciously done to support a narrative that is being established. More on this:

“Two days prior to admission, he was taking phenibut 500mg three times a day and fasoracetam 50-100mg daily. On presentation, he reported that he went to a party and took 10 grams of phenibut”

—This is patently false, and an outright flagrant misrepresentation of the facts. The author has absolutely no idea how much Phenibut I had taken over the first two days. So what did he do? It seems he literally went to a source on Phenibut dosage, found the standard dosage given, and provided this. Moreover, the jump from 1.5g and 1.5, to 10gr, further supports the false narrative of a drastic increase that is of an entire order of magnitude in size. But this is false.

The true dosages, were at about: 4 - 5 g for the first day, 3 - 4 grams on the second, and about 6- 7 grams for the third (the slight increase in dose being explained by the fact that tolerance had already set in, and the drug was not having the same effect on the third day as it had on the first.)

More lies:

“Notably, there were no abnormal pupillary changes”

—This is a lie. I cannot believe how the left hand has no idea what the right hand does or sees, with these systems and institutions. The doctors and nurses were shocked at how big my pupils had been, and ended up measuring pupil changes throughout the period of my stay there in order to assess my condition.

“Physical exam revealed unremarkable respiratory … system [issues]”

Another lie, and a flagrant oversight. In fact, the drastically excessive GABA activation caused by the combination of the potent GABA agonist of Phenibut with the GABA modulating (and upregulating) agent that is Fasoracetam, caused another effect: it lowered my central nervous system’s electrical activity to the point that, for about four days, my lungs had virtually no automatic respiration. As a result, I stayed awake for four days, manually breathing—with the result being that whenever I would stop manually breathing (which would be often), the system monitoring my respiration would ring alarms. I reported this to doctors and nurses over and over—but do you know what they said? “Oh, I’m sure that’s just ‘cause the machine’s malfunctioning.”

Welcome to the incompetence of today’s medical system. To have such a great divergence of reported content, from the actual facts of reality, is astonishing.

“…[patient complained of] … delusions of grandeur”

—Absolutely no such thing of the type was experienced. No such complaint was given; what basis the author or any doctor has for including such a claim is as solid as his basis for claiming that I have had a nonexistent medical history of the mental illness diagnosis of anxiety.

However, the most relevant thing of concern, with the longest-lasting implications to my medical history and subsequent experiences with the medical establishment, is the statement…

“…admitted to the psychiatric unit … for management of his underlying psychosis.”

—What in the blue hell?? *UNDERLYING* psychosis??

Now, this is not the first time in this article that a false claim of diagnosis has been made. (Not to mention that if this publication provided my name as an identifier, the hospital could reasonably be sued for libel.) However, this second claim did not originate with the author, however, as the mistake here originates with what ended up happening at the psychiatric unit.

…

Let us acknowledge one fact: the article makes clear, that this is the first time in medical history, anywhere, that an apparent overdose of Phenibut in combination with Fasoracetam is observed. When you combine two drugs, the truth is, that the “whole” of their effect is often vastly different than the mere sum of their individual parts. This is how people often die using heroin laced with fentanyl, where use of either one alone, even in moderate excess, would not necessitate substantial risk to life.

Similarly, in the case where two new drugs are combined and modern medicine is witnessing the effects under its watchful care for the first time ever, it should be acutely aware (and you think it would be), that the range of what we see In the form of both drug symptoms, and well as drug withdrawal symptoms, can be vastly different in profile and quality than, well…anything you’ve ever necessarily seen before. Novel causes yield novel effects. It’s essentially an “anything goes” scenario, where you didn’t quite know what could result. The article supports this, by stating that various medical symptoms were observed that were not known to have ever been observed in cases of Phenibut overdoses alone—and it accurately ascribed the cause of this to the involvement of the additional substance.

By extension, it is also obviously true, that if anything atypical and out of the ordinary were in fact to be observed, that it would be a direct effect of the combination of drugs taken. If, for example, I reported that I’ve never had a seizure in my life—and then after taking this stuff, I started having a bunch of seizures in the hospital for the first time in my life, right during the apparent withdrawal phase from these drugs…

…You wouldn’t diagnose the patient as having “an underlying SEIZURE disorder!” On your differential diagnosis list, which lists the likely causes of what you’re observing, BY order of probability—at the top of what should be an extremely short list would be “seizures as an apparent after-effect related to (and caused by) the recent administration of these drugs.”

This obvious truth bears doubly-so, if after a reasonable withdrawal period concludes, coinciding with the conclusion of this period Is the permanent cessation of such seizures, which never return again.

Then you would say, “Well no sh*t, Sherlock, you had a *temporary* symptom of seizures, caused by the recent drug combo administration, which was acute.” With the drug gone, and with there no longer being any observable problem, any clinician worth his salt would not attribute the seizures to anything “underlying,” and certainly would not consider the seizures as being pathological in their own right as a seizure disorder truly possessed by the patient, but would instead accurately see them as having been a passing symptom of temporarily-altered neurotransmission caused my the modulation effected by the drugs that were taken. It is accepted and known that this sort of thing typically resolves on its own, and no evidence exists to suggest otherwise for the cases of the substances of Phenibut and Fasoracetam.

To note: Seizures are, in fact, one symptoms of withdrawals from GABAergic drugs.

What I am posing here is a no-brainer.

And addition to this no-brainer, is another no-brainer that I will describe—an important thing to understand when interpreting and assessing situations like this.

(This particular dynamic will come up in a later section of the story, in a shocking way.)

Let’s say you have someone in a given environment. He is yelling, he is screaming. He is moving his hands around, and he is being, well, rowdy.

Is he being manic? Does he have “bipolar disorder?”

Well—let’s provede a little more information for context: This person has had several drinks that evening! And is at a club, or just got out of one, and perhaps has just gotten into or out of a fight, or has hd one of their friends go through the same.

Does this person have a mental disorder? No! Obviously not. Context is key—and in this case, besides the environmental and experiential factors, is the fact that this person has had the drug of alcohol working actively in his system. During both its active phase, as well as during its withdrawal phase, which heightens agitation, the actions, behaviors and mood of the person cannot be accurately ascribed to anything even potentially “underlying,” as the effects of the drug activity and/or post-acute withdrawal supersede In the dominion of manifested behaviors and personality observed.

This is why, as accurately conveyed to me once by someone who has experienced multiple psychiatric unit visits, it is the case that the clinicians and doctors in those kinds of environments, particularly Psychiatric E.R.’s, literally “hate” it when someone gets tossed in there drunk or is obviously on drugs. For people who get syphoned off into Psych ER, they generally throw out the drunks, and do their best to commit the sober people for further investigation. This is because they cannot make a genuine diagnosis of any underlying disorder for the patient, because this person’s native behavior is being masked, and will be masked for some time, by drug activity followed by drug withdrawal phase. The medical and psychiatric authorities recognize this by allocating distinctly different sets of diagnoses—one set for legitimate disorders that are pathological (long-standing illnesses that are in need of long-term treatment), and a separate diagnoses (with separate diagnostic codes) for “temporary” or transient, symptomatic manifestations that are categorically associated with, and understood to be caused by, substance use!

This is key. Can you imagine someone in a setting where they are high on cocaine, and they are seen to be highly energetic as a result.

One diagnosis, of something similar to “Substance-induced agitiation/mania/whatever,” (which follows him for the res of his life) may be given, but such a “diagnosis” is really not a diagnosis at all, because it isn’t really telling you anything about this person’s underlying pathology. From a purely practical standpoint, this person doesn’t have “mental illness”; any future doctor may see, on his universal health record, at best, this reference to the fact that he may have been on drugs once, which caused typical changes to his behavior that it would cause for anyone regardless of health.

Another diagnosis, however, could be extremely damaging. Imagine if, without the context clues, a psychiatrist with one-dimensional thinking made the mistake of observing energetic or aggressive behavior consistent with this person’s cocaine high, or even worse, sees him high one moment and then in low withdrawals the next moment—and proceeded to diagnose him with mood disorder, bipolar disorder or psychosis?

Officially, this one substantial mistake, which happens too often and is too easy to make in today’s psychiatric care system (with lack of safeguards preventing such mindless application of diagnoses), can cause this person to be “red flagged” in the system permanently.

In some states, he can never, ever own weapons again. Anytime he goes to the ER for a legitimate emergency, he is liable to be transferred to psychiatric ER, based on little more than this history, and potentially held against his will for not just 72 hours, but up to 60 days in order to manage his “mental illness.”

This record is seen by every future doctor he ever sees. Any potential future complaint of a legitimate nature may be presented to future doctors—but guess what? If the doctor sees a psychiatric history, he is much more likely to place different weights and assumptions on the list of potential differential diagnoses when assessing your case. This means he is much more likely to lisassume that your symptoms are just “psychosomatic” or the result of mental illness, and you will be separated from proper treatment.

Imagine having a police encounter, for any reason. The difference between being red flagged on a backgroundd check as having mental illness, is the difference between having police take you seriously and diffusing the situation and walking away, and them being “legally compelled” to commit you forcibly to a psychiatric ER, “for mandatory evaluation,” as per simple “protocol.”

Do you think any of these situations listed above are exaggerations? I am speaking from experience when I tell you that, as a result of the initial false seeds planted here in this story, in April 2016, I have unjustly been on the receiving end of every single one of the above situations that I have listed, through no fault of my own. Only false diagnoses and claims backing 100 percent of it, which snowballs into something that is extremely difficult to get yourself out under from. Once you’ve got the labels put on you. If anything, this serves as a stern warning to generally minimize your exposure and interactions with psychiatric and medical entities except whenever necessary, and to generally avoid being accidentally placed in situations that come to shift and morph in ways that are outside of your direct control.

…

To summarize, the reasonable clinician would see, in the presence of drug-related symptoms, both an impediment to making diagnoses about any potential underlying conditions, and ought also to be all the more leaning towards either dismissing any pursuit of legitimate pathology or, at best, assigning an “occurrence of -X- issue as a result of drug intoxication/withdrawal,” so as to not create false misinterpretations and problems for this person further down the road. 

I’ve discussed the insanity and sheer negligence harm of ascribing the wrong diagnosis to someone. However, what was the result of my psychiatric unit stay at NYU?

From the late stages of my ICU stay, to the middle stage of my psychiatric unit stay, it was very apparent about my condition was that I was in some combination of “drug-affected state,” by presence of and/or particularly withdrawal from drug, that resulted in temporary states of significant agitation, worry, and mild hallucinations.

Most notable among these, was the fact that I was concerned, as a result of having high doses of drugs that have been shown in high doses, plus reading one particular case study that a nurse provided, wherein a girl in Russia never woke back up from having a Phenibut overdose, that I was at risk of becoming permanently ill or dying. (A reasonable enough belief to have, when agitation is high and you just came out of a coma.)

Additionally, I found that, for reasons much more deeply explained in my other writings and documents, water seemed to help lessen drug symptoms, by accelerating the rate at which I was able to urinate out the active drug. (This would be relevant, as I would discuss in my later writings how excessive GABA-activation, particularly in the presence of GABA potentiating modulators, have been known to cause conditions where the liver’s metabolic function slows down or ceases completely, causing drugs to linger in the body for significantly longer than expected. This was my experience, both at the hospital and also after the hospital, suggesting longer-term damage that is discussed greatly in my other materials.)

My highest concerns were to remain as assured as possible that I would not end up with complications, and to accelerate the excretion rate of the drugs in my system by drinking water, as withdrawals were in fact effectively accelerated very greatly as immediate effects to increased water intake.

However, the hospital’s idiotic medical staff decided to restrict my water intake, for no legitimate reason other than mindless protocol, to 4 cups of water or less, per day. Because of my being unsatisfied with this, and due to exercising my autonomy in choosing to procure water by “sneaking” it in whichever manner I could, they found my drug/withdrawal-related agitation to be, essentially, a psychiatric event. I was strongly convinced that my life was in legitimate jeopardy given the severity of what I was experiencing, along with the apparent slowness of dissipation, decrease and removal of drug from the system (again, which makes sense pharmacologically, as pro-GABA drugs can often slow down excretion rates by lowering the central nervous system activity levels).

Additionally, I was experiencing an effect known well to doctors as “drug rebound,” which is the (normally) temporary re-emergence of drug symptoms, usually due to diffusion of drug from fat stores; this phenomenon can be greatly accelerated and strengthened due to lipolysis, or fat burn or prolonged fasting states, which was the case for me, as I hadn’t eaten in several days. This strongly lipolytic and ketogenic state likely contributed to recurring waves of drug release that was felt interspersed during my withdrawals, and the lack of stability also caused a legitimate form of worry to onset, which would affect any reasonable person in the situation, especially given that I had no idea that “drug rebound" was possible or that it was in fact a medical occurrence in cases of drug poisoning, and the lack of any other explanation and awareness left me confused and concerned as to what exactly was happening, and why.

The nurses, aides and doctors only saw—from a very “one-dimensional” plane—an occurrence of “man is not perfectly psychologically stable” at this moment. What resulted?

A strong “recommendation” on their part that I take some calming oral medications they were offering, which I voluntarily accepted (only on this one occasion). I proceeded to lie down, and slept.

…

After arising, my mood was calm, and water and food intake helped to stabilize my levels and smooth out my now-tapered withdrawals.

The psychiatrists spent a few more days observing me to make sure there weren’t any more significant events of changes (which there weren’t), and I was granted discharge, much to the great relief of myself and my family.

…

So, in hindsight, what did we experience?

Let’s put it into words as best we can:

A strong GABA agonist known as Phenibut, taken in combination with an upregulating GABA modulator known as Fasoracetam, produced a hypersensitiveing effect on my GABA receptors that resulted in a coma from a few days or relatively moderate Phenibut use (when compared to case studies showing 20 - 25 grams of use and more).

Post-coma, waves of withdrawal interspersed with puzzling drug rebound produced a mix of effects over several days, that eventually manifested as primarily withdrawal-based symptoms that are very “textbook typical” for withdrawal from GABA-based drugs: hallucinations for a few days, significant agitation, mild anxiousness (although this may have been blunted by the Fasoracetam as per its reputation, as most stories I’ve read online about withdrawals from Phenibut sounded much more emotionally horrifying than what I personally experienced), as well as temporary “misinterpretations”, confusion about and misassumptions about situations (caused by temporary withdrawal-based shortages and imbalances of proper neurotransmitters), which are expected with short-term withdrawals from GABA drugs.

Eventually, time helped, and water greatly helped; I stabilized, left the withdrawal phase, and showed regained psychological stability and awareness.

Sounds like your typical GABA-based withdrawal experience.

So, what “mental illness” do we find in the patient? Well, we see that the category of symptoms exhibited were, very clearly, the result of the drug and its textbook series of effects. Understanding that the patient has had absolutely no psych history or mental illness history whatsoever, the window period of alleged or apparent agitation, confusion with added visual hallucinations, are ***CLEARLY*** solely the product of the drug. I don’t know how many more times I can state this without repeating myself excessively.

Honestly, if a person is in that kind of situation dealing with drug effects and withdrawals, there should be no long-standing diagnosis in most situations, as it is difficult to isolate a long-standing, underlying condition from the barrage of intense, immediate, drug-related shifts that are manifesting. As a rule of thumb, most psychiatric sources state that for as long as one month out from most recent drug use, shifts in behavior and symptoms can be attributed to drugs and/or after-effects.

I was handed a discharge paper before leaving—and guess what? There was, in fact, a diagnosis on it.

“Psychosis.”

As in, “this patient is a psychotic person, and suffers from the mental illness of ‘psychosis’.”

I asked the doctor handing me this what this was about, stating strongly that this couldn’t possibly be an even remotely accurate assessment of what has been seen. And his reply was, “Oh don’t worry about that, that’s nothing—that’s just the symptom of what we saw. Doesn’t mean you have the illness.”

………Wow. Hmm. Very disarming words. Nice-sounding words, words that seem to diffuse and explain away the reality of their mistake. I bought it, believing that perhaps this “symptom” didn’t have any ramification on my record or life.

Boy, was I wrong.

Months later, years later even, I log in to my NYU MyChart portal, which is my medical account. Or I got o a doctor who has integrated the medical records of mine. And what does it show on the screen?

“CURRENT DIAGNOSES OF PATIENT:

PSYCHOSIS.”

…

What happened?

Obviously, I am not “sick” today with any underlying psychosis.

Once again, we come to the fact that in these large types of institutions, the left hand doesn't know what the right hand was doing.

The psychiatrists in this completely separate unit and facility weren’t the ones to see the empty drug container, and my body in the coma. They weren’t there to see the positive drug symptoms, the lack of respiration and low heart rate.

They only saw me coming in transferred in as an apparently regular human being, that starts showing large signs of agitation and confusion, with the fact that I had taken something being relegated to the “fine print” within their mental framework of their conscious awareness, in terms of what they understood to be going on.

And as a result, they made a very critical mistake: they rendered a legally harmful and damaging MISDIAGNOSIS.

What is psychosis? Such a diagnosis seems like a stretch. It is normally applied, in legitimate cases, to people that, without apparent subjugation to recent drug effects, exist in a state where, as a result of their underlying mental function, they are unable to maintain normal or appropriate “contact with reality.” This is the extreme form of episodes of delusion or schizophrenic effects.

Would this apply to someone who had extreme withdrawals from drugs? We come again to the philosophical question of differentiating between sadness versus “depression,” anxiousness versus “anxiety,”—the difference between being angry or aggressive and being “manic” with the illness of mania or bipolar disorder, and in this particular case, the difference between being agitated and confused, versus being literally psychotic, which is what the word psychosis means.

Even in the case of the greatest form of “psychotic break,” hallucinations or other such symptoms, if they are the temporary result of drug use, there exists a DUTY for the responsible clinician to render a much more appropriate diagnosis, such as the one on the list of diagnoses known as “Other psychoactive substance use, unspecified with psychoactive substance-induced psychotic disorder, unspecified”.

Two questions arise:

Firstly, do the confusion and agitation I experienced during drug withdrawals qualify , from a medico-legal standpoint, to constitute legitimate psychotic disorder?

Context is key—and, I pose one excellent point in my defense: It’s called a psychotic or mental “disorder,” isn’t it? It is diagnosed as a DIS-order—however, is it really “dis-ordered” to experience these typical, textbook like symptoms as a result of withdrawal from pro-GABA drugs? This isn’t disordered at all; it cannot be disordered if such withdrawals (as per the nurse’s comments before they even kicked in) are literally to be expected! In fact, it is so true, that it would be the lack of expected withdrawal symptoms upon cessation and breakdown of drug matter that would be extremely disordered!

The symptoms we saw cannot be deemed to be a disorder, because they are not out of order to what would reasonably be expected from a well-informed medical standpoint; it is simply understood that, following a large dose of certain types of drugs, agitation, hallucinations and confusion will virtually always reliably follow; therefore, their occurrence cannot be a dis-order of this person’s systems.

Secondly, what do the “psychiatric manuals” (the DSM) state on diagnosing disorders like psychosis—and under what conditions do we diagnose that diagnostic code, as opposed to the “drug-induced” version of it?

Additionally, if we find that the doctors have, in fact, made a mistake, are they legally liable? Have they committed damages? Let’s see what the leading legal sources have to say on this, as we find out! This will be very exciting.

…

In psychiatry, “acute mental confusion” can be used interchangeably with the terms “delirium” or “withdrawal delirium” in more specific circumstances. This term, which is contained within the term delirium tremens, happens to be the same diagnosis given to people withdrawing from large amounts of alcohol, when they manifest the signs.

Would a diagnosis of one drunkard’s delirium tremens follow that person around as a lie long mental illness? No!

I had the “Phenibut + Fasoracetam” version of delirium—so why am I subject to a diagnosis that has much more harmful implications?

Let’s see if, by the definition of psychosis, whether the standard does hold.

…

According to 

…

The criteria for delirium, which generally onsets after withdrawal from a GABA-ergic compounds such as alcohol or others: “Disturbance in attention, awareness, memory, orientation, language, visuospatial ability, perception, or all of these abilities that is a change from the normal level and fluctuates in severity during the day"

I in fact had been experiencing fluctuations in visuospatial ability, along with multiple other factors listed above. Withdrawal delirium, is a delirium that takes place after reduced drug or substance intake.

This would describe it perfectly!

However, does the textbook definition for psychosis (underlying) truly hold?

According to multiple sources, each of the following several criteria for psychosis must be met in other for the diagnosis to be upheld:

From the DSM, on Psychoticdisorder:

“The DSM-5 notes that the clinician must rule out several other conditions to make an accurate diagnosis [for psychotic disorder] (American Psychiatric Association, 2013). Extended abuse of sympathiomimetic agents ( e.g., cocaine and methamphetamine) can result in an acute psychotic break, as can withdrawal from ethanol [or other GABAergic substances] ( Delirium Tremens) and the use of psychedelic agents ( e.g., LSD and psilocybin mushrooms). (Kuzenko, et al 2009). Familiarity with the specific effects of substance use and respective withdrawal syndromes will assist the clinician in making an appropriate differential diagnosis.”

—Wow! It looks like it is written in plain black and white, that it isn’t actually “psychotic disorder” if it has taken place, according to various sources and the DSM, within ONE MONTH of drug use or withdrawal.

(Other support)

Furthermore, the psychiatrist’s claim about the “Psychosis” item listed on the diagnoses section of my discharge papers being only a “symptom,” was disingenuous. As the DSM clearly states that a symptom is a component of an illness, while the diagnoses is the identification of an illness.

So, at the very least, we need to demote this to “Substance-induced psychosis.” But does this diagnosis valid, or is it also incorrect? Let us examine:

From one source: “The Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition(DSM-V) outlines criteria for diagnosing drug-induced psychosis. Five criteria must be met for such a diagnosis to be made. Ultimately, these five criteria are the clearest symptoms of drug-induced psychosis.

(1) Psychotic symptoms cannot be better explained by a pre-existing psychotic disorder, such as schizophrenia or bipolar disorder.

(2) Medical tests have been conducted and confirm that psychotic symptoms presented during substance use or within one month of withdrawing from the substance.

(3) Delusions and/or hallucinations are present.

(4) Psychotic symptoms are consistent and do not occur only during states of delirium.

(5) Psychotic symptoms are having a significant impact on the individual’s ability to function in daily life and causing great distress.


All of the above criteria must be met for a formal diagnosis of drug-induced psychosis to be made.”

So are all of these above five points truly met?

The first three points are valid: the issues at hand could not have been better explained by “underlying psychosis.” It was reported and taken as fact that this was after drug use.As for the third point, whether hallucinations and delusions being present, it is arguable based on how these terms are defined. We may come back to this.

But what matters, ultimately, is the total inapplicability of the remaining two points, which categorically disqualifies “any type” of psychosis as being an appropriate diagnosis!

Let us examine. The first three seem valid. However, the fourth point is where the diagnosis shows its unsuitability for my case. Psychotic symptoms, in my case, where most definitively not “consistent,” as they were limited to the period of apparent withdrawal delirium.

Additionally, the fifth point also fails to be met; no such symptoms were having any significant impact on my “daily life,” as this was an extremely temporary withdrawal phase experienced, in its entirety, through the period of only about 3 - 4 days while in a hospital. The issue was not long-term enough to be a “daily life” factor, and was completely resolved before I was discharged.


Additionally, an additional note is provided following these five points in the original material, as a kind of unofficial 6th point:

The diagnosis can ONLY be made when the symptoms are “substantially in excess of what would be expected given the type or amount of the substance used or the duration of use.”

But because the amounts and combinations of drug in my case would, in fact, likely result in comparable behaviors and temporary disorders of confusion or perception for anyone else in the same position and with the same drug dosages and timeframes.

Medicine has only support for this position of mine by its knowledge of GABAergic withdrawal dynamics, and NO evidence to the contrary, as they have no evidence that Phenibut and Fasoracetam combinations DON’T produce the exact type f withdrawal dynamics that I went though—because I’m the only recorded case of it.

Is there evidence that Phenibut causes psychotic symptoms during withdrawal? Yes. The same sources quoted earlier on Phenibut withdrawals also lists psychosis as one of them, where in context, it is understood that it is part of the expected dynamic.

Moreover, to summarize, what the DSM and related body of knowledge states, is that “Phenibut is known to cause psychosis so it can’t be underlying—so maybe it’s drug-induced. Oh, but it isn’t really “drug-induced psychosis,” since our own body of knowledge already acknowledges these types of things to be within the expected range of dynamics—so really there isn’t any diagnosable condition at all.”

That’s right.

The only diagnosis they could have pushed, that would have been reasonable, would have been “substance use, substance withdrawal,” and a the most, “withdrawal delirium” or other comparable diagnosis.

Under no situation should I be looking at any papers from present-day medical records and health accounts, and see labels and false claims showing “This patient suffer from psychotic disorder that is surely present and active.”

…

The poor guy who wrote the Fasoracetam article—he looks at the psychiatric record after my discharge, all he sees Is “Psychosis” given as the diagnosis, understands that in the normal codes and without any context, this is taken by default to be understood as “underlying psychosis,” and puts this false statement in the report.

This follows me around everywhere.

…

So, what can we do about it?

The laws in this country protect people both from having false statements made about them that are harmful, and particularly, also offer protections against people who are given false diagnoses and made to believe them or otherwise “suffer by its effects.”

Let’s take a particularly close look at the latter.

According to a legal source on medical malpractice, two elements must be proved by a doctor’s patient in order to have a successful claim: in short, negligence, and harm.

A doctor is considered negligent when “a doctor in a similar specialty, under similar circumstances, [and acting with reasonable precaution], would not have provided a wrongful diagnosis for a patient’s condition.” This is usually done by some failure to consider the appropriate diagnosis in what is called the “differential diagnosis” list, and by errors of reasoning, ultimately selected the wrong diagnosis, in cases where they, in short, “should have known better.”

In this case, the psychiatric team had both enough information about my case and its context, as well as the criteria and requirements of the set of potential diagnoses, in order to come to the correct conclusion. Therefore, there are grounds to claim that the doctors acted negligently in failing to include the proper diagnoses on the differential list, and failing to find that the diagnosis they applied did not have all required criteria met.

Additionally, are there damages? Legal precedent says ‘yes’. 

There are two ways in which harm and damages have accrued. The first is in the case of wrongful diagnosis, particularly wrongful mental diagnosis, is considered harmful in that it may be presumed to have caused the patient “anxiety and stress,” which roughly summarizes my experience of being placed on this label.

Additionally, the second element, beyond affecting reputation, also causes future doctors to place different or altered weights on consideration of various candidates on their own respective differential diagnoses lists, thus affecting the quality of care I have received in the last three years, in the form of many doctors being caused to be dismissive of legitimate symptoms, and prolonging or delaying treatment as a result of reported “psych information” that they believed to be true, but is, in actuality, false.

…

What would a poor-quality clinician in their position do (—likely just as they did?)

They may see the situation, and say “All I know, is that I see a patient who was admitted here, and for some reason, has exhibited signs of hallucinations (which we did not check to see if he is “aware” of their false nature, which is a disqualifying condition for hallucination in the DSM) and other symptoms. I see that the patient shows signs of confusion, agitation, and possibly delusion. I have not established any proper context to these symptoms, and I have not bothered to find out whether this patient has never before had any such symptoms of behaviors prior to admission. I have not made any connection to substance use, so therefore, we will assume he is suffering from psychotic disorder, which must be underlying. I will also not bother double-checking the diagnostic criteria to make sure whether this can be ruled out—and we’ll put it as a diagnosis, while telling him it’s just a symptom, although this is not what doctors in the future will see.”

This leaves the psychiatrist one little diagnostic criteria away from getting a law suit. It’s scary. But what would a responsible, well-ordered clinician see?

“I see a patient came in who took a combination of drugs that no one in modern medical history has seen anyone take the combination of. We see he is suffering from symptoms that include elements of confusion, possibly delusion, agitation, and other such related issues. However, I have investigated with the patient and his family, and found that none of these types of behaviors have ever been displayed by the patient. This, in combination with the fact that we do have a working understanding of roughly what kind of withdrawal symptoms we see in people withdrawn from pro-GABA agents, leads me to belief that the most probable assessment of the reality of his situation isn’t of any underlying psychosis, or even necessarily psychosis at all, but rather, part of the elements of confusion and poor interpretation of environment that comes with withdrawal delirium.

Furthermore, because we have no concrete evidence of medical precedent to show that his withdrawal symptoms are in excess of the withdrawals that would biochemically be expected from his particular drug combination (after all, it was clearly a strong enough dose to put him into a coma), we must assume that the full spectrum of behaviors and symptoms witnessed are a part of the rebound withdrawals. Therefore, no version of psychotic diagnosis would be applicable, as multiple criteria for such a diagnosis are clearly not met, and thus we are left to diagnose only substance use withdrawal and possibly withdrawal delirium, which is also symptomatic, and essentially isn’t a diagnosis of any underlying condition either. Research into the drug Phenibut confirms that withdrawals include symptoms of both confusion, agitation as well as psychosis, thus further cementing the fact that these are all within the normal parameters of Phenibut withdrawals. Since Fasoracetam is a potentiator, the withdrawals may have likely been potentiated too; thus, no symptoms exhibited can be definitely perceived as being beyond the expected range of such an instance of psychoactive drug poisoning and withdrawal. To prevent confusion to any future doctors, I should not place diagnoses that can be misinterpreted out of context in any manner.”

Wow! This is a clinician who is worth the money put into his degree.

…

Questions for both the clinician or psychologist/psychiatrist, and legal expert to address:

(1) Do you support the conclusion that the original diagnosis of “[underlying] psychosis” is, based on all available evidence and facts, a misdiagnosis?

(2) What full, underlying diagnoses would better be suited to replace the diagnosis of “psychosis/psychotic disorder” that was given?

(3) Do we have reason to believe that the doctor may have been negligent in his diagnostic process, taking too little care to ensure that the proper, most-fitting diagnosis is rendered and that, even more importantly, that diagnoses that do not fit are effectively eliminated from consideration?

(4) Do you support and encourage the petitioning of the doctors and the hospital for them to GO BACK TO THE RECORDS AND CHANGE THE DIAGNOSIS to a more appropriate one?

I apologize for the formatting, I have copied and pasted the text, nd it has come up in this manner.

Thank you for your time.

"NYU - APRIL 2016

During the spring of 2016, I was planning to try a particularly pure and well-reputed version of a little-known Soviet-created “smart drug,” an anxiolytic substance that I had dabbled with before in the past in a recreational manner—a substance known as Phenibut.

As an “over the counter,” non-regulated pro-GABA drug, it acts similarly to alcohol or to benzodiazepines, except without as strong of a factor of sedation.

The Phenibut drug had seen an increase in recreational use in recent years by this time. While it was known to be particularly effective at making social events and parties more enjoyable, some online communities had began discussing the potential concurrent use of a second type of nootropic or smart drug known as Fasoracetam. This drug is believed to work in some kind of synergistic manner to Phenibut, as some people reported that it seems to reduce the negative after-effects of Phenibut use.

To note: As these are two drugs both relatively unknown to Western pharmacology, with on of them being Soviet-invented and the other having been invented relatively recently, there were absolutely no case studies or reported information in the medical literature on what happens when anyone combines these two in amounts.

What were the dosage standards? Brand name Russian Phenibut, which is called (R)-Phenibut (being the only psychoactive enantiomer compared to racemic (R,S)-Phenibut), is recommended up to XXXXXXX dose of 2,250mg daily. Extrapolating this dose to racemic Phenibut, which was the version I possessed, this would logically double to 4,450 mg XXXXXXX dose per day, as this amount of racemic Phenibut contains 2,250 mg of the psychoactive portion, which is the (R)-enantiomer of the drug.

Recreational doses, according to many sources online, go northwards from 2 -3 grams per day, and often reach as high as 7 - 10 grams per day with some users. I decided I would definitely stay below the 7 - 10 gram range, as this is close to double the recommended XXXXXXX dose that is intended for daily use.

With Fasoracetam, the recommended dosages, according to most sources and literature available at the time, seemed. to be more flexible, and ultimately less restrictive. Various sources showed a large range of dosage, ranging from 100 mg per day, to upwards of 800 mg per day, to be safe for dosage. I decided I would not consume more than “roughly a few hundred milligrams” of this second substance per day as well.

According to all material available to me at the time, there were no indications to show that users taking Phenibut recreationally experienced any significant danger or damage. The same applied to Fasoracetam, which was considered to be largely much more safe in comparison as well. Additionally, there were limited anecdotal reports available by users who had indicated that they use the mixture of the two drug with no problem or adverse effects to report.

Therefore, I decided I would conduct a limited testing of these drugs over a three-day period, during which I consumed on each day (or each evening, with daily doses broken down and taken over the course of several hours): approximately a few grams of Phenibut each evening, along with a few hundred milligrams of Fasoracetam.

After the first two days of use, no ill reports or side effects were noted. While I presumed to conclude that this meant that these I decided I would dose for one additional evening on the third day using only slightly higher amounts than those used on the first two days, before planning to take a few days of break to allow these drugs to cycle out of my system and report findings to the online nootropic (smart drug) community.

However, after by the end of the third evening, I lost consciousness—and ended up in a coma at a local hospital by morning.

…

**********
“Phenibut Overdose in Combination with Fasoracetam: Emerging Drugs of Abuse - jcicm-aid1001.pdf”
https://www.heighpubs.org/jcicm/pdf/jcicm-aid1001.pdf
**********

My story, according to the relevant research departments at this hospital:


INTRODUCTION

“The widespread availability of non-traditional dietary supplements and pharmacologically active substances via the Internet continues to introduce mechanisms for inadvertent toxidromes not commonly seen. Consumers are virtually unrestricted in their ability to acquire products purporting augmentation of normal physiology for the purposes of enhancement, recreation, and/or potential abuse. The safety profiles at standard or toxic doses remain largely unknown for many agents that can be purchased electronically. We report a case of mixed toxicity related to phenibut and fosaracetam, both of which are readily available for consumer purchase from online retailers. Written and verbal consent was obtained for this case presentation.

CASE REPORT 

“A 27-year-old male with a past medical history of anxiety was discovered unresponsive on the sidewalk. Paramedics responding to the scene noted that the patient had an initial Glascow Coma Score (GCS) of 3 and possessed an empty 5 gram bottle of fasoracetam. During transport to our institution, there were brief periods of severe agitation with emesis. On arrival to our emergency department (ED), the patient exhibited intermittent episodes of agitation and disorientation only upon physical stimulation. Physical exam revealed unremarkable respiratory, abdominal, and musculoskeletal systems. Notably, there were no abnormal pupillary changes or clonus. His vital signs were characterized by normal blood pressure of 135/62 mm Hg, respiratory rate of 12 breaths/min, and an oxygen saturation of 95% on room air. The most signiβicant βinding was a sinus bradycardia with a heart rate of 36 beats/min, for which the patient received 0.5 mg atropine sulfate resulting in a short-lived response to 70 beats/min. All laboratory measurements were within normal limits. Levels for acetaminophen, digoxin, salicylate, and ethanol were not detected. Bedside urine toxicology immunoassay was negative for benzodiazepines, tricyclic antidepressants, cocaine, amphetamines, tetrahydrocannabinol, opioids, barbiturates, phencyclidine and ketamine. A non-contrast CT head ruled out any contributing intracranial pathology.

“While in the ED, the patient remained somnolent, and persistently bradycardic with heart rates ranging from 34 to 50 beats/min requiring placement of transcutaneous pacing pads. The patient displayed amnesia to all events preceding his presentation. He acknowledged that his current state deviated from his normal baseline neurologic and functional status. The patient denied any recent illicit, prescription, or over-the counter drug use, reported social alcohol consumption, and recent use of fasoracetam to enhance mental capacitance and alertness.

“After 24 hours, the patient was able to recall that he purchased phenibut 99.5% powder 100 grams, and fasoracetam powder 5 grams through LiftMode and Nootropics Depot with the intention to stabilize his ‘GABA system’. Two days prior to admission, he was taking phenibut 500mg three times a day and fasoracetam 50-100mg daily. On presentation, he reported that he went to a party and took 10 grams of phenibut and an unknown amount of fasoracetam. On hospital day 2, his lethargy and bradycardia was mostly resolved but complained about increasing anxiety, hallucinations, and delusions of grandeur. He was evaluated by the psychiatric team, and was admitted to the psychiatric unit for evaluation and management of his underlying psychosis. 

DISCUSSION

“Racemic phenibut is a GABAB agonist that possesses anxiolytic and nootropic activity mainly attributed to its R-enantiomer [1]. It is structurally similar to baclofen but differs by the presence of one chlorine atom in the benzene ring and is 30 times less active as a GABAB agonist [2]. Other pharmacological activity includes decreasing the activity of voltage-dependent Ca2+ ionic channels similarly to gabapentin and possibly GABAA agonism at high doses [1,2]. Limited information is available on the pharmacokinetics of phenibut. After systemic absorption, phenibut is rapidly distributed to the brain, kidneys, liver, and urine. The elimination half life is 5.3 hours and 65% of the parent drug is excreted into the urine [1,2].

“All published acute toxicities from phenibut are summarized in Table 1 [3-9]. Oral administration of phenibut was the most common route with doses ranging from 1 gram to 30 grams with single oral administration. The onset of desired effects was reported to occur within 2-4 hours following oral ingestion with an overall duration of 7-24 hours. Most patients presented with altered mental status, low levels of consciousness, and agitation upon arousal. In cases characterized by severe agitation, benzodiazepines and antipsychotics demonstrated minimal to moderate effects. All patients were carefully monitored in either an emergency observation or intensive care unit and most were discharged within 24-48 hours from admission.

“In contrast to previously reported cases, our patient was also taking fasoracetam which stimulates metabotropic glutamate receptors, up-regulates GABAB receptors, and stimulates the release of acetylcholine from central cholinergic neurons [10]. It is absorbed rapidly after oral administration and has a bioavailability of 79%-97%. The elimination half-life ranges from 4-6.5 hours and is predominately excreted in the urine as unchanged drug [10]. Fasoracetam (NFC-1) has recently obtained an Investigational New Drug (IND) from the Food and Drug Administration to be evaluated in patients with ADHD who have rare glutamate gene mutation and has a well-established safety profile from previous clinical trials at recommended doses (50-800mg a day in divided doses) [10]. The most commonly reported side effects include headache and fatigue. Nevertheless, large doses of fasoracetam could potentially explain the bradycardia experienced by this patient as it is not seen with the reported cases of phenibut overdoses. In addition, fasoracetam could potentially enhance the response to phenibut through the up-regulation of GABAB receptors and decrease the threshold for tolerance that is commonly observed with phenibut.

“Phenibut and fasoracetam are widely available from internet sites that are mainly based in the UK and USA [2,8]. These unregulated products place the general public at risk from overdoses and can produce unique toxidromes especially with co-administration of multiple supplements. The clinical management is primarily supportive, but should incorporate a thorough history of recent medication use, including dietary supplements and vitamins. In the majority of phenibut overdoses, the toxicological properties predominantly effects the central nervous system and to a lesser extent the cardiovascular system. Healthcare providers should be prepared to manage or inform patients about the acute excess or withdrawal side effects after phenibut or fasoracetam overdoses [11].”

…

The article above does a satisfactory job of conveying the gist of what happened. I was found unconscious in public and brought into NYU Hospital in New York, where I remained in a coma for about 12 or so hours. Once I awoke, I proceeded to be observed for a few days in Step-down from ICU unit.

A few things of importance also took place during the first few days, as well as during the subsequent days, that all tie in to a certain body of information, as well as into a narrative regarding an ongoing state of health that I have been dealing with to this day, on the medical aspect. The medical side of the story, and the after-effects that I have been living with, is a side of the story that I discuss much more deeply in a separate set of documents that I have compiled over the last three years. The information presented therein in slightly out of the scope of this document, as I am here to present more of the procedural aspects of what happened, in the context of mis-diagnoses within the psychiatric domain. I encourage the interested reader to read my other documents for more information on what happened in the hospital, as well as ongoing issues stemming from the use of these drugs.

The relevant portions of the story, however, I will describe below.

…

A day or two prior to being discharged from the ER/ICU side of the hospital, I agreed to undergo voluntary admission into the hospital’s psychiatric unit, in order to be observed and to be able to manage any potential withdrawals from these drugs, and to also give the hospital a chance to make sure that I’m fully recovered and stabilized at the psychological level.

Importantly: I have had absolutely no prior medical history of mental illness whatsoever, with no mental diagnosis being made, through up until this time being in the hospital. Moreover, I have been functional through up until this time, with there being no assumption, no suspicion, no evidence and no accusation of mental illness or mental illness symptoms present anywhere in the past or present, in my life.

Moreover, according to all information available on the post-effects of Phenibut and/or Fasoracetam, on the development of mental illness?

There is none whatsoever; all discharges reported in the other related cases summarized above make implication that no further evidence or psychological damage was present at all, as the effects of the drug are transient and largely benign psychologcally—this is with the exception of one particular aspect, that is important to highlight.

When I spoke to the nurses during my ER/ICU stay, they asked me how I felt. When I told them I felt very good, they kind of laughed, and remarked among themselves, saying, “Just wait till the withdrawals start kicking in…”

Another nurse, wishing to tip me off on what would likely be happening, printed out a medical document and showed me something that basically mirrored what the following quote from the Maryland Poison Control Center states:

“Withdrawal symptoms [from Phenibut], which can last two weeks or longer, may include anxiety, agitation, fatigue, hallucinations, … In addition, symptoms for which phenibut was taken will return. Treatment includes supportive care and benzodiazepines for agitation.”

—Hallucinations!! Imagine that.

Most people in general associate hallucinations with two things: legitimate mental disorders, and also hallucinations as part of the positive drug effects given from hallucinogenic drugs like LSD.

However, fewer people understand that, while hallucinogenic drug gives you hallucinations when you’re on them, other types of drugs—notably the GABAergic type, of which Phenibut is one (along with alcohol, bentos and others)—can produce hallucinations and delirium tremens when you are gong OFF of these drugs! This is due to the short-lived exposure of tolerance and down regulated GABA receptors, once drug level begin to lower. It is after a short period of time that these receptors reset back to their default setting only in, and following, the absence of the drug, and the person returns to normal function.

I am glad that this nurse tipped me off, because I had no idea at that time that something like this was possible. Surely enough, the withdrawals, consisting of agitation and hallucinations too, stated to kick in. In addition to these symptoms were symptoms of delusion or false-belief, which go hand-in-hand with GABAergic withdrawal patterns, and is clearly understood by competent professionals to be distinctly limited to the withdrawal phase in otherwise-normal population.

After a few days, and before the withdrawals completely subsided, I had transferred to the psychiatric facility. But before we proceed to discuss how this ended up turning out, I’d like to address the Phenibut + Fasoracetam article mentioned above—as in it, we can see the first instances and causes of what would be a cascading series of mistakes and problems the results of which I would inherit and still be dealing with to this day.

Firstly, to note: We have the subconscious belief, as humans, to take those publications from sources we deem as being authoritative, and consider the information inside as being nothing else other than gospel truth.

Well, after I came across this article months after it was published without my awareness, I was shocked to find at how many pieces of information that they got wrong.

Let us examine.

…

“[The patient] possessed an empty 5-gram [container] of fasoracetam.”

This is true, and in fact gave the ER dept the first large clue that my coma and lack of consciousness was drug-induced—in fact, It was the only clue that they had, as none of their drug tests could uncover the fact that I had multiple such drugs in my system.

However, what was the initial assumption made by the team when they see an unconscious person with an empty drug container? They think I took all of it at once, and that it could have likely been a suicide attempt. (Which isn’t true at all, and I quickly and truthfully refuted this assumption by anyone who posed it.)

“…an unknown amount of Fasoracetam.”

This is a lie. I clearly reported to the doctors and staff the approximate amounts taken, which was within the range I specified, furthermore, this amount was roughly consistent with the amount taken on each of the other two days.

“…a past medical history of anxiety”

This is a complete, bold lie, and it is the most dangerous lie that likely started the problems. After all, I had earlier just explained to the reader, that I have had absolutely no past “medical” history of hardly anything. I also did not make statements about “having anxiety,” which are words that we should be very careful when using, and I shall explain why.

Consider this: what is the difference between sadness and depression? One of them is a normal human emotion that can be experienced regularly—the other is a psychiatric disorder and a mental illness. It is important to note that, of course, only a doctor can diagnose someone with a mental illness. The same goes with any of the others—do you get anxious sometimes, or do you have [the diagnosed mental illness] of anxiety?

An additional quirk of the XXXXXXX system—only a drug (or FDA approved therapy or procedure) can cure or treat illness of any kind, including mental illness, which means that once a mental illness is officially diagnosed, it is “accepted” that it can never legally or medically be “cured”—it can just either “go into remission,” or have it be found that you were “misdiagnosed” in the first place if it is apparent that the illness is not present in a patient.

In fact, making claims that a person “has” any kind of mental illness without it actually being true that the person was factually diagnosed with such an illness? This can cause a person to face court charges for defamation under the law, as our society is very protective of slander and libel, which is what this essentially is.

Keep in mind that at no point during this stay with NYU did anyone ever diagnose me with anxiety. How was this lie of “past medical history of anxiety” constructed for inclusion in an article like this? Allow me to paint the picture: It is as simple as a guy who looks up what Phenibut is generally used for, he finds out that it can “treat anxiety,” and simply goes, “Oh, it must be ‘cause he’s got anxiety!”

A past history of sadness is not the same as a past history of depression. Moreover, a past history of depression is not the same as a past medical history of depression, where n the latter case, as opposed to the former presumably, the supposed depression would be medically documented and diagnosed, and thus legitimately pre-established. Thus, there are multiple layers to the insanity and boldness of this falsity.

Why does this take place? This is subconsciously done to support a narrative that is being established. More on this:

“Two days prior to admission, he was taking phenibut 500mg three times a day and fasoracetam 50-100mg daily. On presentation, he reported that he went to a party and took 10 grams of phenibut”

—This is patently false, and an outright flagrant misrepresentation of the facts. The author has absolutely no idea how much Phenibut I had taken over the first two days. So what did he do? It seems he literally went to a source on Phenibut dosage, found the standard dosage given, and provided this. Moreover, the jump from 1.5g and 1.5, to 10gr, further supports the false narrative of a drastic increase that is of an entire order of magnitude in size. But this is false.

The true dosages, were at about: 4 - 5 g for the first day, 3 - 4 grams on the second, and about 6- 7 grams for the third (the slight increase in dose being explained by the fact that tolerance had already set in, and the drug was not having the same effect on the third day as it had on the first.)

More lies:

“Notably, there were no abnormal pupillary changes”

—This is a lie. I cannot believe how the left hand has no idea what the right hand does or sees, with these systems and institutions. The doctors and nurses were shocked at how big my pupils had been, and ended up measuring pupil changes throughout the period of my stay there in order to assess my condition.

“Physical exam revealed unremarkable respiratory … system [issues]”

Another lie, and a flagrant oversight. In fact, the drastically excessive GABA activation caused by the combination of the potent GABA agonist of Phenibut with the GABA modulating (and upregulating) agent that is Fasoracetam, caused another effect: it lowered my central nervous system’s electrical activity to the point that, for about four days, my lungs had virtually no automatic respiration. As a result, I stayed awake for four days, manually breathing—with the result being that whenever I would stop manually breathing (which would be often), the system monitoring my respiration would ring alarms. I reported this to doctors and nurses over and over—but do you know what they said? “Oh, I’m sure that’s just ‘cause the machine’s malfunctioning.”

Welcome to the incompetence of today’s medical system. To have such a great divergence of reported content, from the actual facts of reality, is astonishing.

“…[patient complained of] … delusions of grandeur”

—Absolutely no such thing of the type was experienced. No such complaint was given; what basis the author or any doctor has for including such a claim is as solid as his basis for claiming that I have had a nonexistent medical history of the mental illness diagnosis of anxiety.

However, the most relevant thing of concern, with the longest-lasting implications to my medical history and subsequent experiences with the medical establishment, is the statement…

“…admitted to the psychiatric unit … for management of his underlying psychosis.”

—What in the blue hell?? *UNDERLYING* psychosis??

Now, this is not the first time in this article that a false claim of diagnosis has been made. (Not to mention that if this publication provided my name as an identifier, the hospital could reasonably be sued for libel.) However, this second claim did not originate with the author, however, as the mistake here originates with what ended up happening at the psychiatric unit.

…

Let us acknowledge one fact: the article makes clear, that this is the first time in medical history, anywhere, that an apparent overdose of Phenibut in combination with Fasoracetam is observed. When you combine two drugs, the truth is, that the “whole” of their effect is often vastly different than the mere sum of their individual parts. This is how people often die using heroin laced with fentanyl, where use of either one alone, even in moderate excess, would not necessitate substantial risk to life.

Similarly, in the case where two new drugs are combined and modern medicine is witnessing the effects under its watchful care for the first time ever, it should be acutely aware (and you think it would be), that the range of what we see In the form of both drug symptoms, and well as drug withdrawal symptoms, can be vastly different in profile and quality than, well…anything you’ve ever necessarily seen before. Novel causes yield novel effects. It’s essentially an “anything goes” scenario, where you didn’t quite know what could result. The article supports this, by stating that various medical symptoms were observed that were not known to have ever been observed in cases of Phenibut overdoses alone—and it accurately ascribed the cause of this to the involvement of the additional substance.

By extension, it is also obviously true, that if anything atypical and out of the ordinary were in fact to be observed, that it would be a direct effect of the combination of drugs taken. If, for example, I reported that I’ve never had a seizure in my life—and then after taking this stuff, I started having a bunch of seizures in the hospital for the first time in my life, right during the apparent withdrawal phase from these drugs…

…You wouldn’t diagnose the patient as having “an underlying SEIZURE disorder!” On your differential diagnosis list, which lists the likely causes of what you’re observing, BY order of probability—at the top of what should be an extremely short list would be “seizures as an apparent after-effect related to (and caused by) the recent administration of these drugs.”

This obvious truth bears doubly-so, if after a reasonable withdrawal period concludes, coinciding with the conclusion of this period Is the permanent cessation of such seizures, which never return again.

Then you would say, “Well no sh*t, Sherlock, you had a *temporary* symptom of seizures, caused by the recent drug combo administration, which was acute.” With the drug gone, and with there no longer being any observable problem, any clinician worth his salt would not attribute the seizures to anything “underlying,” and certainly would not consider the seizures as being pathological in their own right as a seizure disorder truly possessed by the patient, but would instead accurately see them as having been a passing symptom of temporarily-altered neurotransmission caused my the modulation effected by the drugs that were taken. It is accepted and known that this sort of thing typically resolves on its own, and no evidence exists to suggest otherwise for the cases of the substances of Phenibut and Fasoracetam.

To note: Seizures are, in fact, one symptoms of withdrawals from GABAergic drugs.

What I am posing here is a no-brainer.

And addition to this no-brainer, is another no-brainer that I will describe—an important thing to understand when interpreting and assessing situations like this.

(This particular dynamic will come up in a later section of the story, in a shocking way.)

Let’s say you have someone in a given environment. He is yelling, he is screaming. He is moving his hands around, and he is being, well, rowdy.

Is he being manic? Does he have “bipolar disorder?”

Well—let’s provede a little more information for context: This person has had several drinks that evening! And is at a club, or just got out of one, and perhaps has just gotten into or out of a fight, or has hd one of their friends go through the same.

Does this person have a mental disorder? No! Obviously not. Context is key—and in this case, besides the environmental and experiential factors, is the fact that this person has had the drug of alcohol working actively in his system. During both its active phase, as well as during its withdrawal phase, which heightens agitation, the actions, behaviors and mood of the person cannot be accurately ascribed to anything even potentially “underlying,” as the effects of the drug activity and/or post-acute withdrawal supersede In the dominion of manifested behaviors and personality observed.

This is why, as accurately conveyed to me once by someone who has experienced multiple psychiatric unit visits, it is the case that the clinicians and doctors in those kinds of environments, particularly Psychiatric E.R.’s, literally “hate” it when someone gets tossed in there drunk or is obviously on drugs. For people who get syphoned off into Psych ER, they generally throw out the drunks, and do their best to commit the sober people for further investigation. This is because they cannot make a genuine diagnosis of any underlying disorder for the patient, because this person’s native behavior is being masked, and will be masked for some time, by drug activity followed by drug withdrawal phase. The medical and psychiatric authorities recognize this by allocating distinctly different sets of diagnoses—one set for legitimate disorders that are pathological (long-standing illnesses that are in need of long-term treatment), and a separate diagnoses (with separate diagnostic codes) for “temporary” or transient, symptomatic manifestations that are categorically associated with, and understood to be caused by, substance use!

This is key. Can you imagine someone in a setting where they are high on cocaine, and they are seen to be highly energetic as a result.

One diagnosis, of something similar to “Substance-induced agitiation/mania/whatever,” (which follows him for the res of his life) may be given, but such a “diagnosis” is really not a diagnosis at all, because it isn’t really telling you anything about this person’s underlying pathology. From a purely practical standpoint, this person doesn’t have “mental illness”; any future doctor may see, on his universal health record, at best, this reference to the fact that he may have been on drugs once, which caused typical changes to his behavior that it would cause for anyone regardless of health.

Another diagnosis, however, could be extremely damaging. Imagine if, without the context clues, a psychiatrist with one-dimensional thinking made the mistake of observing energetic or aggressive behavior consistent with this person’s cocaine high, or even worse, sees him high one moment and then in low withdrawals the next moment—and proceeded to diagnose him with mood disorder, bipolar disorder or psychosis?

Officially, this one substantial mistake, which happens too often and is too easy to make in today’s psychiatric care system (with lack of safeguards preventing such mindless application of diagnoses), can cause this person to be “red flagged” in the system permanently.

In some states, he can never, ever own weapons again. Anytime he goes to the ER for a legitimate emergency, he is liable to be transferred to psychiatric ER, based on little more than this history, and potentially held against his will for not just 72 hours, but up to 60 days in order to manage his “mental illness.”

This record is seen by every future doctor he ever sees. Any potential future complaint of a legitimate nature may be presented to future doctors—but guess what? If the doctor sees a psychiatric history, he is much more likely to place different weights and assumptions on the list of potential differential diagnoses when assessing your case. This means he is much more likely to lisassume that your symptoms are just “psychosomatic” or the result of mental illness, and you will be separated from proper treatment.

Imagine having a police encounter, for any reason. The difference between being red flagged on a backgroundd check as having mental illness, is the difference between having police take you seriously and diffusing the situation and walking away, and them being “legally compelled” to commit you forcibly to a psychiatric ER, “for mandatory evaluation,” as per simple “protocol.”

Do you think any of these situations listed above are exaggerations? I am speaking from experience when I tell you that, as a result of the initial false seeds planted here in this story, in April 2016, I have unjustly been on the receiving end of every single one of the above situations that I have listed, through no fault of my own. Only false diagnoses and claims backing 100 percent of it, which snowballs into something that is extremely difficult to get yourself out under from. Once you’ve got the labels put on you. If anything, this serves as a stern warning to generally minimize your exposure and interactions with psychiatric and medical entities except whenever necessary, and to generally avoid being accidentally placed in situations that come to shift and morph in ways that are outside of your direct control.

…

To summarize, the reasonable clinician would see, in the presence of drug-related symptoms, both an impediment to making diagnoses about any potential underlying conditions, and ought also to be all the more leaning towards either dismissing any pursuit of legitimate pathology or, at best, assigning an “occurrence of -X- issue as a result of drug intoxication/withdrawal,” so as to not create false misinterpretations and problems for this person further down the road. 

I’ve discussed the insanity and sheer negligence harm of ascribing the wrong diagnosis to someone. However, what was the result of my psychiatric unit stay at NYU?

From the late stages of my ICU stay, to the middle stage of my psychiatric unit stay, it was very apparent about my condition was that I was in some combination of “drug-affected state,” by presence of and/or particularly withdrawal from drug, that resulted in temporary states of significant agitation, worry, and mild hallucinations.

Most notable among these, was the fact that I was concerned, as a result of having high doses of drugs that have been shown in high doses, plus reading one particular case study that a nurse provided, wherein a girl in Russia never woke back up from having a Phenibut overdose, that I was at risk of becoming permanently ill or dying. (A reasonable enough belief to have, when agitation is high and you just came out of a coma.)

Additionally, I found that, for reasons much more deeply explained in my other writings and documents, water seemed to help lessen drug symptoms, by accelerating the rate at which I was able to urinate out the active drug. (This would be relevant, as I would discuss in my later writings how excessive GABA-activation, particularly in the presence of GABA potentiating modulators, have been known to cause conditions where the liver’s metabolic function slows down or ceases completely, causing drugs to linger in the body for significantly longer than expected. This was my experience, both at the hospital and also after the hospital, suggesting longer-term damage that is discussed greatly in my other materials.)

My highest concerns were to remain as assured as possible that I would not end up with complications, and to accelerate the excretion rate of the drugs in my system by drinking water, as withdrawals were in fact effectively accelerated very greatly as immediate effects to increased water intake.

However, the hospital’s idiotic medical staff decided to restrict my water intake, for no legitimate reason other than mindless protocol, to 4 cups of water or less, per day. Because of my being unsatisfied with this, and due to exercising my autonomy in choosing to procure water by “sneaking” it in whichever manner I could, they found my drug/withdrawal-related agitation to be, essentially, a psychiatric event. I was strongly convinced that my life was in legitimate jeopardy given the severity of what I was experiencing, along with the apparent slowness of dissipation, decrease and removal of drug from the system (again, which makes sense pharmacologically, as pro-GABA drugs can often slow down excretion rates by lowering the central nervous system activity levels).

Additionally, I was experiencing an effect known well to doctors as “drug rebound,” which is the (normally) temporary re-emergence of drug symptoms, usually due to diffusion of drug from fat stores; this phenomenon can be greatly accelerated and strengthened due to lipolysis, or fat burn or prolonged fasting states, which was the case for me, as I hadn’t eaten in several days. This strongly lipolytic and ketogenic state likely contributed to recurring waves of drug release that was felt interspersed during my withdrawals, and the lack of stability also caused a legitimate form of worry to onset, which would affect any reasonable person in the situation, especially given that I had no idea that “drug rebound" was possible or that it was in fact a medical occurrence in cases of drug poisoning, and the lack of any other explanation and awareness left me confused and concerned as to what exactly was happening, and why.

The nurses, aides and doctors only saw—from a very “one-dimensional” plane—an occurrence of “man is not perfectly psychologically stable” at this moment. What resulted?

A strong “recommendation” on their part that I take some calming oral medications they were offering, which I voluntarily accepted (only on this one occasion). I proceeded to lie down, and slept.

…

After arising, my mood was calm, and water and food intake helped to stabilize my levels and smooth out my now-tapered withdrawals.

The psychiatrists spent a few more days observing me to make sure there weren’t any more significant events of changes (which there weren’t), and I was granted discharge, much to the great relief of myself and my family.

…

So, in hindsight, what did we experience?

Let’s put it into words as best we can:

A strong GABA agonist known as Phenibut, taken in combination with an upregulating GABA modulator known as Fasoracetam, produced a hypersensitiveing effect on my GABA receptors that resulted in a coma from a few days or relatively moderate Phenibut use (when compared to case studies showing 20 - 25 grams of use and more).

Post-coma, waves of withdrawal interspersed with puzzling drug rebound produced a mix of effects over several days, that eventually manifested as primarily withdrawal-based symptoms that are very “textbook typical” for withdrawal from GABA-based drugs: hallucinations for a few days, significant agitation, mild anxiousness (although this may have been blunted by the Fasoracetam as per its reputation, as most stories I’ve read online about withdrawals from Phenibut sounded much more emotionally horrifying than what I personally experienced), as well as temporary “misinterpretations”, confusion about and misassumptions about situations (caused by temporary withdrawal-based shortages and imbalances of proper neurotransmitters), which are expected with short-term withdrawals from GABA drugs.

Eventually, time helped, and water greatly helped; I stabilized, left the withdrawal phase, and showed regained psychological stability and awareness.

Sounds like your typical GABA-based withdrawal experience.

So, what “mental illness” do we find in the patient? Well, we see that the category of symptoms exhibited were, very clearly, the result of the drug and its textbook series of effects. Understanding that the patient has had absolutely no psych history or mental illness history whatsoever, the window period of alleged or apparent agitation, confusion with added visual hallucinations, are ***CLEARLY*** solely the product of the drug. I don’t know how many more times I can state this without repeating myself excessively.

Honestly, if a person is in that kind of situation dealing with drug effects and withdrawals, there should be no long-standing diagnosis in most situations, as it is difficult to isolate a long-standing, underlying condition from the barrage of intense, immediate, drug-related shifts that are manifesting. As a rule of thumb, most psychiatric sources state that for as long as one month out from most recent drug use, shifts in behavior and symptoms can be attributed to drugs and/or after-effects.

I was handed a discharge paper before leaving—and guess what? There was, in fact, a diagnosis on it.

“Psychosis.”

As in, “this patient is a psychotic person, and suffers from the mental illness of ‘psychosis’.”

I asked the doctor handing me this what this was about, stating strongly that this couldn’t possibly be an even remotely accurate assessment of what has been seen. And his reply was, “Oh don’t worry about that, that’s nothing—that’s just the symptom of what we saw. Doesn’t mean you have the illness.”

………Wow. Hmm. Very disarming words. Nice-sounding words, words that seem to diffuse and explain away the reality of their mistake. I bought it, believing that perhaps this “symptom” didn’t have any ramification on my record or life.

Boy, was I wrong.

Months later, years later even, I log in to my NYU MyChart portal, which is my medical account. Or I got o a doctor who has integrated the medical records of mine. And what does it show on the screen?

“CURRENT DIAGNOSES OF PATIENT:

PSYCHOSIS.”

…

What happened?

Obviously, I am not “sick” today with any underlying psychosis.

Once again, we come to the fact that in these large types of institutions, the left hand doesn't know what the right hand was doing.

The psychiatrists in this completely separate unit and facility weren’t the ones to see the empty drug container, and my body in the coma. They weren’t there to see the positive drug symptoms, the lack of respiration and low heart rate.

They only saw me coming in transferred in as an apparently regular human being, that starts showing large signs of agitation and confusion, with the fact that I had taken something being relegated to the “fine print” within their mental framework of their conscious awareness, in terms of what they understood to be going on.

And as a result, they made a very critical mistake: they rendered a legally harmful and damaging MISDIAGNOSIS.

What is psychosis? Such a diagnosis seems like a stretch. It is normally applied, in legitimate cases, to people that, without apparent subjugation to recent drug effects, exist in a state where, as a result of their underlying mental function, they are unable to maintain normal or appropriate “contact with reality.” This is the extreme form of episodes of delusion or schizophrenic effects.

Would this apply to someone who had extreme withdrawals from drugs? We come again to the philosophical question of differentiating between sadness versus “depression,” anxiousness versus “anxiety,”—the difference between being angry or aggressive and being “manic” with the illness of mania or bipolar disorder, and in this particular case, the difference between being agitated and confused, versus being literally psychotic, which is what the word psychosis means.

Even in the case of the greatest form of “psychotic break,” hallucinations or other such symptoms, if they are the temporary result of drug use, there exists a DUTY for the responsible clinician to render a much more appropriate diagnosis, such as the one on the list of diagnoses known as “Other psychoactive substance use, unspecified with psychoactive substance-induced psychotic disorder, unspecified”.

Two questions arise:

Firstly, do the confusion and agitation I experienced during drug withdrawals qualify , from a medico-legal standpoint, to constitute legitimate psychotic disorder?

Context is key—and, I pose one excellent point in my defense: It’s called a psychotic or mental “disorder,” isn’t it? It is diagnosed as a DIS-order—however, is it really “dis-ordered” to experience these typical, textbook like symptoms as a result of withdrawal from pro-GABA drugs? This isn’t disordered at all; it cannot be disordered if such withdrawals (as per the nurse’s comments before they even kicked in) are literally to be expected! In fact, it is so true, that it would be the lack of expected withdrawal symptoms upon cessation and breakdown of drug matter that would be extremely disordered!

The symptoms we saw cannot be deemed to be a disorder, because they are not out of order to what would reasonably be expected from a well-informed medical standpoint; it is simply understood that, following a large dose of certain types of drugs, agitation, hallucinations and confusion will virtually always reliably follow; therefore, their occurrence cannot be a dis-order of this person’s systems.

Secondly, what do the “psychiatric manuals” (the DSM) state on diagnosing disorders like psychosis—and under what conditions do we diagnose that diagnostic code, as opposed to the “drug-induced” version of it?

Additionally, if we find that the doctors have, in fact, made a mistake, are they legally liable? Have they committed damages? Let’s see what the leading legal sources have to say on this, as we find out! This will be very exciting.

…

In psychiatry, “acute mental confusion” can be used interchangeably with the terms “delirium” or “withdrawal delirium” in more specific circumstances. This term, which is contained within the term delirium tremens, happens to be the same diagnosis given to people withdrawing from large amounts of alcohol, when they manifest the signs.

Would a diagnosis of one drunkard’s delirium tremens follow that person around as a lie long mental illness? No!

I had the “Phenibut + Fasoracetam” version of delirium—so why am I subject to a diagnosis that has much more harmful implications?

Let’s see if, by the definition of psychosis, whether the standard does hold.

…

According to 

…

The criteria for delirium, which generally onsets after withdrawal from a GABA-ergic compounds such as alcohol or others: “Disturbance in attention, awareness, memory, orientation, language, visuospatial ability, perception, or all of these abilities that is a change from the normal level and fluctuates in severity during the day"

I in fact had been experiencing fluctuations in visuospatial ability, along with multiple other factors listed above. Withdrawal delirium, is a delirium that takes place after reduced drug or substance intake.

This would describe it perfectly!

However, does the textbook definition for psychosis (underlying) truly hold?

According to multiple sources, each of the following several criteria for psychosis must be met in other for the diagnosis to be upheld:

From the DSM, on Psychoticdisorder:

“The DSM-5 notes that the clinician must rule out several other conditions to make an accurate diagnosis [for psychotic disorder] (American Psychiatric Association, 2013). Extended abuse of sympathiomimetic agents ( e.g., cocaine and methamphetamine) can result in an acute psychotic break, as can withdrawal from ethanol [or other GABAergic substances] ( Delirium Tremens) and the use of psychedelic agents ( e.g., LSD and psilocybin mushrooms). (Kuzenko, et al 2009). Familiarity with the specific effects of substance use and respective withdrawal syndromes will assist the clinician in making an appropriate differential diagnosis.”

—Wow! It looks like it is written in plain black and white, that it isn’t actually “psychotic disorder” if it has taken place, according to various sources and the DSM, within ONE MONTH of drug use or withdrawal.

(Other support)

Furthermore, the psychiatrist’s claim about the “Psychosis” item listed on the diagnoses section of my discharge papers being only a “symptom,” was disingenuous. As the DSM clearly states that a symptom is a component of an illness, while the diagnoses is the identification of an illness.

So, at the very least, we need to demote this to “Substance-induced psychosis.” But does this diagnosis valid, or is it also incorrect? Let us examine:

From one source: “The Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition(DSM-V) outlines criteria for diagnosing drug-induced psychosis. Five criteria must be met for such a diagnosis to be made. Ultimately, these five criteria are the clearest symptoms of drug-induced psychosis.

(1) Psychotic symptoms cannot be better explained by a pre-existing psychotic disorder, such as schizophrenia or bipolar disorder.

(2) Medical tests have been conducted and confirm that psychotic symptoms presented during substance use or within one month of withdrawing from the substance.

(3) Delusions and/or hallucinations are present.

(4) Psychotic symptoms are consistent and do not occur only during states of delirium.

(5) Psychotic symptoms are having a significant impact on the individual’s ability to function in daily life and causing great distress.


All of the above criteria must be met for a formal diagnosis of drug-induced psychosis to be made.”

So are all of these above five points truly met?

The first three points are valid: the issues at hand could not have been better explained by “underlying psychosis.” It was reported and taken as fact that this was after drug use.As for the third point, whether hallucinations and delusions being present, it is arguable based on how these terms are defined. We may come back to this.

But what matters, ultimately, is the total inapplicability of the remaining two points, which categorically disqualifies “any type” of psychosis as being an appropriate diagnosis!

Let us examine. The first three seem valid. However, the fourth point is where the diagnosis shows its unsuitability for my case. Psychotic symptoms, in my case, where most definitively not “consistent,” as they were limited to the period of apparent withdrawal delirium.

Additionally, the fifth point also fails to be met; no such symptoms were having any significant impact on my “daily life,” as this was an extremely temporary withdrawal phase experienced, in its entirety, through the period of only about 3 - 4 days while in a hospital. The issue was not long-term enough to be a “daily life” factor, and was completely resolved before I was discharged.


Additionally, an additional note is provided following these five points in the original material, as a kind of unofficial 6th point:

The diagnosis can ONLY be made when the symptoms are “substantially in excess of what would be expected given the type or amount of the substance used or the duration of use.”

But because the amounts and combinations of drug in my case would, in fact, likely result in comparable behaviors and temporary disorders of confusion or perception for anyone else in the same position and with the same drug dosages and timeframes.

Medicine has only support for this position of mine by its knowledge of GABAergic withdrawal dynamics, and NO evidence to the contrary, as they have no evidence that Phenibut and Fasoracetam combinations DON’T produce the exact type f withdrawal dynamics that I went though—because I’m the only recorded case of it.

Is there evidence that Phenibut causes psychotic symptoms during withdrawal? Yes. The same sources quoted earlier on Phenibut withdrawals also lists psychosis as one of them, where in context, it is understood that it is part of the expected dynamic.

Moreover, to summarize, what the DSM and related body of knowledge states, is that “Phenibut is known to cause psychosis so it can’t be underlying—so maybe it’s drug-induced. Oh, but it isn’t really “drug-induced psychosis,” since our own body of knowledge already acknowledges these types of things to be within the expected range of dynamics—so really there isn’t any diagnosable condition at all.”

That’s right.

The only diagnosis they could have pushed, that would have been reasonable, would have been “substance use, substance withdrawal,” and a the most, “withdrawal delirium” or other comparable diagnosis.

Under no situation should I be looking at any papers from present-day medical records and health accounts, and see labels and false claims showing “This patient suffer from psychotic disorder that is surely present and active.”

…

The poor guy who wrote the Fasoracetam article—he looks at the psychiatric record after my discharge, all he sees Is “Psychosis” given as the diagnosis, understands that in the normal codes and without any context, this is taken by default to be understood as “underlying psychosis,” and puts this false statement in the report.

This follows me around everywhere.

…

So, what can we do about it?

The laws in this country protect people both from having false statements made about them that are harmful, and particularly, also offer protections against people who are given false diagnoses and made to believe them or otherwise “suffer by its effects.”

Let’s take a particularly close look at the latter.

According to a legal source on medical malpractice, two elements must be proved by a doctor’s patient in order to have a successful claim: in short, negligence, and harm.

A doctor is considered negligent when “a doctor in a similar specialty, under similar circumstances, [and acting with reasonable precaution], would not have provided a wrongful diagnosis for a patient’s condition.” This is usually done by some failure to consider the appropriate diagnosis in what is called the “differential diagnosis” list, and by errors of reasoning, ultimately selected the wrong diagnosis, in cases where they, in short, “should have known better.”

In this case, the psychiatric team had both enough information about my case and its context, as well as the criteria and requirements of the set of potential diagnoses, in order to come to the correct conclusion. Therefore, there are grounds to claim that the doctors acted negligently in failing to include the proper diagnoses on the differential list, and failing to find that the diagnosis they applied did not have all required criteria met.

Additionally, are there damages? Legal precedent says ‘yes’. 

There are two ways in which harm and damages have accrued. The first is in the case of wrongful diagnosis, particularly wrongful mental diagnosis, is considered harmful in that it may be presumed to have caused the patient “anxiety and stress,” which roughly summarizes my experience of being placed on this label.

Additionally, the second element, beyond affecting reputation, also causes future doctors to place different or altered weights on consideration of various candidates on their own respective differential diagnoses lists, thus affecting the quality of care I have received in the last three years, in the form of many doctors being caused to be dismissive of legitimate symptoms, and prolonging or delaying treatment as a result of reported “psych information” that they believed to be true, but is, in actuality, false.

…

What would a poor-quality clinician in their position do (—likely just as they did?)

They may see the situation, and say “All I know, is that I see a patient who was admitted here, and for some reason, has exhibited signs of hallucinations (which we did not check to see if he is “aware” of their false nature, which is a disqualifying condition for hallucination in the DSM) and other symptoms. I see that the patient shows signs of confusion, agitation, and possibly delusion. I have not established any proper context to these symptoms, and I have not bothered to find out whether this patient has never before had any such symptoms of behaviors prior to admission. I have not made any connection to substance use, so therefore, we will assume he is suffering from psychotic disorder, which must be underlying. I will also not bother double-checking the diagnostic criteria to make sure whether this can be ruled out—and we’ll put it as a diagnosis, while telling him it’s just a symptom, although this is not what doctors in the future will see.”

This leaves the psychiatrist one little diagnostic criteria away from getting a law suit. It’s scary. But what would a responsible, well-ordered clinician see?

“I see a patient came in who took a combination of drugs that no one in modern medical history has seen anyone take the combination of. We see he is suffering from symptoms that include elements of confusion, possibly delusion, agitation, and other such related issues. However, I have investigated with the patient and his family, and found that none of these types of behaviors have ever been displayed by the patient. This, in combination with the fact that we do have a working understanding of roughly what kind of withdrawal symptoms we see in people withdrawn from pro-GABA agents, leads me to belief that the most probable assessment of the reality of his situation isn’t of any underlying psychosis, or even necessarily psychosis at all, but rather, part of the elements of confusion and poor interpretation of environment that comes with withdrawal delirium.

Furthermore, because we have no concrete evidence of medical precedent to show that his withdrawal symptoms are in excess of the withdrawals that would biochemically be expected from his particular drug combination (after all, it was clearly a strong enough dose to put him into a coma), we must assume that the full spectrum of behaviors and symptoms witnessed are a part of the rebound withdrawals. Therefore, no version of psychotic diagnosis would be applicable, as multiple criteria for such a diagnosis are clearly not met, and thus we are left to diagnose only substance use withdrawal and possibly withdrawal delirium, which is also symptomatic, and essentially isn’t a diagnosis of any underlying condition either. Research into the drug Phenibut confirms that withdrawals include symptoms of both confusion, agitation as well as psychosis, thus further cementing the fact that these are all within the normal parameters of Phenibut withdrawals. Since Fasoracetam is a potentiator, the withdrawals may have likely been potentiated too; thus, no symptoms exhibited can be definitely perceived as being beyond the expected range of such an instance of psychoactive drug poisoning and withdrawal. To prevent confusion to any future doctors, I should not place diagnoses that can be misinterpreted out of context in any manner.”

Wow! This is a clinician who is worth the money put into his degree.

…

Questions for both the clinician or psychologist/psychiatrist, and legal expert to address:

(1) Do you support the conclusion that the original diagnosis of “[underlying] psychosis” is, based on all available evidence and facts, a misdiagnosis?

(2) What full, underlying diagnoses would better be suited to replace the diagnosis of “psychosis/psychotic disorder” that was given?

(3) Do we have reason to believe that the doctor may have been negligent in his diagnostic process, taking too little care to ensure that the proper, most-fitting diagnosis is rendered and that, even more importantly, that diagnoses that do not fit are effectively eliminated from consideration?

(4) Do you support and encourage the petitioning of the doctors and the hospital for them to GO BACK TO THE RECORDS AND CHANGE THE DIAGNOSIS to a more appropriate one?