Question: Hi, attached to this are documents pertaining to my case of suspected H.E, caused by poisoning of GABAergic drugs. Please take the time to evaluate and read very carefully.

Questions to consider after reading:

How likely does it seem to be the case that I may have underlying dysfunction consistent with that found in hepatic encephalopathy? Can any remaining barriers to a confirmed diagnosis, if any, be overcome by the application of a presumptive diagnosis? Following your analysis, would you support with a favorable opinion the securing of a presumptive diagnosis for Type A (neurologically-based) hepatic encephalopathy (caused by excessive GABAergic tone?)

Thank you.

Hi, attached to this are documents pertaining to my case of suspected H.E, caused by poisoning of GABAergic drugs. Please take the time to evaluate and read very carefully.

Questions to consider after reading:

How likely does it seem to be the case that I may have underlying dysfunction consistent with that found in hepatic encephalopathy? Can any remaining barriers to a confirmed diagnosis, if any, be overcome by the application of a presumptive diagnosis? Following your analysis, would you support with a favorable opinion the securing of a presumptive diagnosis for Type A (neurologically-based) hepatic encephalopathy (caused by excessive GABAergic tone?)

Thank you.

Okay, just sent to you. Thank you

Okay, just sent to you. Thank you

Thank God for you,

You have given me the best and most rationally sane and extremely helpful answer on this website. I am extremely glad you were the one to answer.
I am going to go back to my doctors and tell them that I have favorable opinion and support from a doctor in another country, that has read my material.

Please tell me what is your specialty/background? Is it just pharmacology? Are you a general doctor, neurologist, any other type?

I do have additional information regarding this case. It is more lengthy, unfortunately, than these.

Please allow me a short bit of time to consider what else I can pose or ask, and how such questions and answers may be favorable to me.

Thank you very much once again

Thank God for you,

You have given me the best and most rationally sane and extremely helpful answer on this website. I am extremely glad you were the one to answer.
I am going to go back to my doctors and tell them that I have favorable opinion and support from a doctor in another country, that has read my material.

Please tell me what is your specialty/background? Is it just pharmacology? Are you a general doctor, neurologist, any other type?

I do have additional information regarding this case. It is more lengthy, unfortunately, than these.

Please allow me a short bit of time to consider what else I can pose or ask, and how such questions and answers may be favorable to me.

Thank you very much once again

Reports attached

Reports attached

Hi,

Justo to follow up:

(1) I have sent you a list of symptoms, for further opinion and commentary by you.

(2) To note: Unfortunately, for the last three years, doing nothing has not produced any beneficial effect upon the liver. I speculate that this is likely as a result of the perpetual and chronic up-modulating effect and pressure that Fasoracetam exerts by its continued presence, thus keeping GABAergic tone effectively elevated. This also counters the natural tendency of the body to downregulate in response to excessive neurotransmittory tone, which is a dangerous thing.

(3) Only GABA inhibitors have shown (temporary) improvements in symptoms.

(4) Flumazenil is the drug common used to antagonize GABA-A receptors, which is the receptor type most often associated with excessive stimulation in cases of HE and other drug poisonings. However, in my case, both drugs exert their primary effect uniquely on GABA-B, and NOT on GABA A. Therefore, which GABA-B antagonists are most suitable for use?

(5) Moreover, since Fasoracetam's upregulating effect on GABA is not via direct antagonism, but bby some other downstream effect or resultant upmodulation, we may need other approaches to stop Fasoracetam. By my research, it seems that it is a direct cholinergic substance, first and foremost. Would applying cholinergic blockers be a good approach, at least theoretically, to counter the downstream effects of Fasoracetam?

(6) I have come up with a theory, based on my case--it is that, in addition to exerting inhibition and disablement of the microsomes of the liver via CNS level reduction, there is ALSO a neural based and likely CNS-mediated mechanism that regulates the activity of the kidneys.

I have multiple supporting evidence for this: (1) Ever since poisoning, my urine has become much lighter, never darker yellow and never cloudy, regardless of how much proteins I consume; (2) extremely low amino acid yields in urine, as evidenced by lab tests; (3) the standalone fact that most Fasoracetam normally appears unchanged and unmetabolized in urine, implying that liver action is not neessary for its effective excretion, but that kidneys must work; and, (4) I have found a study, "Renal Denervation Improves the Baroreflex and GABA System in Chronic Kidney Disease-induced Hypertension", which indicates that (a) GABA-B receptor increase is associated with impaired kidney function; (b) cutting or denerving the kidneys restores kidney function partially. Fasoracetam, as we know, upregulates GABA-B density; therefore, it is not a far stretch to imagine that it inhibits not only the liver by its action, but also the activity of the kidney's glomerules; (5) when I take large amounts of GABA-inhibitors and tryptophan, it is only ever then that my urine temporarily restores its darker color and cloudiness (and thus, its normal excretory yield) that I have known throughout my whle life before the poisoning.

My theory is that in addition to GABA-induced CNS depression inducing hepatic encephalopathy (and "lung" encephalopathy by reducing its reflex to draw in air), it also induces a kind of "renal encephalopathy'--which is a functional reduction in kidney waste processing, although it of course remains effectively masked (much like my liver condition vis-a-vis "mostly normal" LFTs) by its inherent inflammation-suppressing and damage-suppressing actions.

Please let me know what you think, and how to go about informing and educationg the medical establishment about these un-realized dynamics, and the best way to cure the condition. Thank you.

Hi,

Justo to follow up:

(1) I have sent you a list of symptoms, for further opinion and commentary by you.

(2) To note: Unfortunately, for the last three years, doing nothing has not produced any beneficial effect upon the liver. I speculate that this is likely as a result of the perpetual and chronic up-modulating effect and pressure that Fasoracetam exerts by its continued presence, thus keeping GABAergic tone effectively elevated. This also counters the natural tendency of the body to downregulate in response to excessive neurotransmittory tone, which is a dangerous thing.

(3) Only GABA inhibitors have shown (temporary) improvements in symptoms.

(4) Flumazenil is the drug common used to antagonize GABA-A receptors, which is the receptor type most often associated with excessive stimulation in cases of HE and other drug poisonings. However, in my case, both drugs exert their primary effect uniquely on GABA-B, and NOT on GABA A. Therefore, which GABA-B antagonists are most suitable for use?

(5) Moreover, since Fasoracetam's upregulating effect on GABA is not via direct antagonism, but bby some other downstream effect or resultant upmodulation, we may need other approaches to stop Fasoracetam. By my research, it seems that it is a direct cholinergic substance, first and foremost. Would applying cholinergic blockers be a good approach, at least theoretically, to counter the downstream effects of Fasoracetam?

(6) I have come up with a theory, based on my case--it is that, in addition to exerting inhibition and disablement of the microsomes of the liver via CNS level reduction, there is ALSO a neural based and likely CNS-mediated mechanism that regulates the activity of the kidneys.

I have multiple supporting evidence for this: (1) Ever since poisoning, my urine has become much lighter, never darker yellow and never cloudy, regardless of how much proteins I consume; (2) extremely low amino acid yields in urine, as evidenced by lab tests; (3) the standalone fact that most Fasoracetam normally appears unchanged and unmetabolized in urine, implying that liver action is not neessary for its effective excretion, but that kidneys must work; and, (4) I have found a study, "Renal Denervation Improves the Baroreflex and GABA System in Chronic Kidney Disease-induced Hypertension", which indicates that (a) GABA-B receptor increase is associated with impaired kidney function; (b) cutting or denerving the kidneys restores kidney function partially. Fasoracetam, as we know, upregulates GABA-B density; therefore, it is not a far stretch to imagine that it inhibits not only the liver by its action, but also the activity of the kidney's glomerules; (5) when I take large amounts of GABA-inhibitors and tryptophan, it is only ever then that my urine temporarily restores its darker color and cloudiness (and thus, its normal excretory yield) that I have known throughout my whle life before the poisoning.

My theory is that in addition to GABA-induced CNS depression inducing hepatic encephalopathy (and "lung" encephalopathy by reducing its reflex to draw in air), it also induces a kind of "renal encephalopathy'--which is a functional reduction in kidney waste processing, although it of course remains effectively masked (much like my liver condition vis-a-vis "mostly normal" LFTs) by its inherent inflammation-suppressing and damage-suppressing actions.

Please let me know what you think, and how to go about informing and educationg the medical establishment about these un-realized dynamics, and the best way to cure the condition. Thank you.

I fully agree with your last statement, that only the absence of the disturbing chemicals would allow for proper neurokinetic and regulatory dynamics--this is why, as part of my petition to doctors around me, I have firmly pushed for the use of hemoperfusion.

The list of evidence from my documents can be reviewed for a reminder as to how likely it is that these drugs do continue to actively saturate the tissues and nervous system.

(A) Given our understanding, would you support and advocate for the use of hemoperfusion in a custom, unique case like mine, give that (1) hemoperfusion is demonstrated to be effective in reversing broad-spectrum of known cases of poisoning, and (2) hemoperfusion is demonstrated in studies to be effective for reversing and improving condition of Hepatic Encephalopathy, regardless of which type?


(B) There further details, which I would love to discuss. I believe this website might limit the amount of responses we provide to each other before communication is automatically cut-off, as seems to be the case from previous discussions with other doctors. Given this, if you are interested in learning more about this case, I would be happy to send you more information through any means that you wish. I highly value your opinion and your interest in my case ***as you are the firs doctor I have contacted in three years who takes my case seriously.*** THANK YOU.

(C) I do have additional details that would, in fact, require the input of research scientists. I would appreciate any help with coordiating the matter, as I am not sure where to turn first. Most notably out of the spectrum of standard medicine, is a particular dynamic of physics that I have researched, that I feel well explains the continued presence of drug within the system--this is BEYOND the mere neural inhibition caused by excessive GABAergic tone, and has to do with a dynamic called "CPA," or crystallization by particle attachment (as per De Yoreo et al, 2015), which describes how saturated precipitated material within any system has the propensity to take ions from the surrounding environment, in order to literally grow.

The liver my counter most manifestations of this, such that it is normally not noticeable within a healthy organism; however, I have compied a compelling case that multiple friends have read, and fully believe.

I am the first one ever, as far as I can tell, who has proposed these theories. If accepted by the scientific community, this would be a real game-changer.

. . .

Thank you again, Doctor.

Thank you so much.

. . .

Additionall

I fully agree with your last statement, that only the absence of the disturbing chemicals would allow for proper neurokinetic and regulatory dynamics--this is why, as part of my petition to doctors around me, I have firmly pushed for the use of hemoperfusion.

The list of evidence from my documents can be reviewed for a reminder as to how likely it is that these drugs do continue to actively saturate the tissues and nervous system.

(A) Given our understanding, would you support and advocate for the use of hemoperfusion in a custom, unique case like mine, give that (1) hemoperfusion is demonstrated to be effective in reversing broad-spectrum of known cases of poisoning, and (2) hemoperfusion is demonstrated in studies to be effective for reversing and improving condition of Hepatic Encephalopathy, regardless of which type?


(B) There further details, which I would love to discuss. I believe this website might limit the amount of responses we provide to each other before communication is automatically cut-off, as seems to be the case from previous discussions with other doctors. Given this, if you are interested in learning more about this case, I would be happy to send you more information through any means that you wish. I highly value your opinion and your interest in my case ***as you are the firs doctor I have contacted in three years who takes my case seriously.*** THANK YOU.

(C) I do have additional details that would, in fact, require the input of research scientists. I would appreciate any help with coordiating the matter, as I am not sure where to turn first. Most notably out of the spectrum of standard medicine, is a particular dynamic of physics that I have researched, that I feel well explains the continued presence of drug within the system--this is BEYOND the mere neural inhibition caused by excessive GABAergic tone, and has to do with a dynamic called "CPA," or crystallization by particle attachment (as per De Yoreo et al, 2015), which describes how saturated precipitated material within any system has the propensity to take ions from the surrounding environment, in order to literally grow.

The liver my counter most manifestations of this, such that it is normally not noticeable within a healthy organism; however, I have compied a compelling case that multiple friends have read, and fully believe.

I am the first one ever, as far as I can tell, who has proposed these theories. If accepted by the scientific community, this would be a real game-changer.

. . .

Thank you again, Doctor.

Thank you so much.

. . .

Additionall

Thank you for your reply.

Yes, hemoperfusion would be most effective if there were sill drugs in the body. It would be a scary implication to have continued Fasoracetam-like upregulation and Phenibut (and cocaine + other drugs) effects lingering for years if they were gone. It would also be more difficult scientifically to explain such a phenomenon.

Due to the fact that I can still smell many of the drugs in my system, especially from my sweat, along with continued localized anesthetization effect of cocaine on mucous membranes for a year and a half, and smell and effects of Phenibut, among others, that are my biggest clues that the drugs still remain. (Other also smell alcohol from me almost a week after drinking--though alcohol eventually dissipates via evaporation and urination/sweat, the most quickly compared to other substances.

Additionally, I have the private proof, done with family as witness, showing positive cocaine saliva test 12 days after use, where all scientific sources show that traces cannot remain longer than 48 hours in the saliva in a person with normal, healthy metabolism.

. . .

Yes, I am afraid the situaiton has forcibly made me enthusiastic about fixing this problem. For it is my life, truly, that is ultimately on the line.

What I admire about you is your ability to grab the sense of reality from a convoluted, complex and unique problem. Many people do not have this ability. The dialogue shown between mysef and the other GI doc, depicted in the documents, is a testament to that fact.

I would be most excited to share with you a couple of special sets of documents that I have shown close friends who have been in support of me.

I have produced three "sets" of documents, that I've been compiling and maintaining over the years, since this happened:

the A set, which is a kind of summary or introduction,

the B set, which goes a little bit deeper,

and the C set, which is the set of original, unedited chronicles and logs that I maintain and update with medical issues and also my explanations.

I would love to send you, to start, both the A set (documents A02 - A05) and the B set, and see what you think about the overall case. I will send it via the attachments email service.

I greatly appreciate your involvement and interest in my case. Perhaps at the conclusion, once we have assessed the whole case, we can have the best ideas and conclusion as to which direction to head to.

Thank you.

-Jon

Thank you for your reply.

Yes, hemoperfusion would be most effective if there were sill drugs in the body. It would be a scary implication to have continued Fasoracetam-like upregulation and Phenibut (and cocaine + other drugs) effects lingering for years if they were gone. It would also be more difficult scientifically to explain such a phenomenon.

Due to the fact that I can still smell many of the drugs in my system, especially from my sweat, along with continued localized anesthetization effect of cocaine on mucous membranes for a year and a half, and smell and effects of Phenibut, among others, that are my biggest clues that the drugs still remain. (Other also smell alcohol from me almost a week after drinking--though alcohol eventually dissipates via evaporation and urination/sweat, the most quickly compared to other substances.

Additionally, I have the private proof, done with family as witness, showing positive cocaine saliva test 12 days after use, where all scientific sources show that traces cannot remain longer than 48 hours in the saliva in a person with normal, healthy metabolism.

. . .

Yes, I am afraid the situaiton has forcibly made me enthusiastic about fixing this problem. For it is my life, truly, that is ultimately on the line.

What I admire about you is your ability to grab the sense of reality from a convoluted, complex and unique problem. Many people do not have this ability. The dialogue shown between mysef and the other GI doc, depicted in the documents, is a testament to that fact.

I would be most excited to share with you a couple of special sets of documents that I have shown close friends who have been in support of me.

I have produced three "sets" of documents, that I've been compiling and maintaining over the years, since this happened:

the A set, which is a kind of summary or introduction,

the B set, which goes a little bit deeper,

and the C set, which is the set of original, unedited chronicles and logs that I maintain and update with medical issues and also my explanations.

I would love to send you, to start, both the A set (documents A02 - A05) and the B set, and see what you think about the overall case. I will send it via the attachments email service.

I greatly appreciate your involvement and interest in my case. Perhaps at the conclusion, once we have assessed the whole case, we can have the best ideas and conclusion as to which direction to head to.

Thank you.

-Jon

Hi Doctor--

Yes, these testimonies are the only validation I have attained to far--but unfortunately, because they are not from doctors, it hasn't opened up any miraculous paths of access to treatment for me.

The doctor's letter, honestly, was drafted by me. My primary care doctor, after reading it and engaging in minor rounds of back-and-forth editing, reluctantly signed it, as it was the best representation of what he felt was "plausible"--but in truth, in the year-plus since the time of his signing it, he has not taken the care to fully analyze the details, and till this day in his heart believes that I must be mistaken about most of these assumptions and conclusions.

It is sad to see, because to myself and to multiple friends, the issues seems obvious.

. . .

I would be very curious what you think of the deeper details outlined in the B-set, once you have had time to carefully read through and conclude your assessment of their contents.

Do you believe that all aspects of what is presented are plausible? If so, how can I strengthen support and recognition for their status? If not, when what details do you feel may be missing? If you were to play "Devil's advocate," where do you see weak spots or alternative explanations for what I see, obvserve, experience, hypothesize and report?

(On the matter of drugs remaining in the body at higher concentrations--indeed: cocaine is one such known drug that, in higher accumulations within normally-elastic intestinal tissue, is well-known by its use to be associated with intestinal tears. Such tears have been experienced by me, as reported on extensively in various documents, yet no doctor believes it because I have (1) pain, (2) inflammation, and (3) immune response all effectively blocked--these three indicators are the ONLY indicators that doctors can use with normal population to determine acute abdomen.

On the matter of drug detox protocols: yes, besides an actual hemoperfusion-type or M.A.R.S.-type set-up, the only other way is to use saunas, often with high-dose niacin, as recomended by a well-known MD (urologist and surgeon) within the detox community, Dr XXXXXXX Yu. This tactic works on people who have almost an type of toxin with does not directly neurologically interfere with the metabolic/excretory system functions, vis-a-vis the CNS. But in my case, past use of saunas and niacin have caused such massive releases of Phenibut/Fasoracetam drug, and effects, that the net progress is aactually negative, as the liver becomes more slowed as a result of the stronger circulatory presence and redistribution of fat-stored drug.)

Thank you for your dedication doctor. Your support means a lot to me.

Hi Doctor--

Yes, these testimonies are the only validation I have attained to far--but unfortunately, because they are not from doctors, it hasn't opened up any miraculous paths of access to treatment for me.

The doctor's letter, honestly, was drafted by me. My primary care doctor, after reading it and engaging in minor rounds of back-and-forth editing, reluctantly signed it, as it was the best representation of what he felt was "plausible"--but in truth, in the year-plus since the time of his signing it, he has not taken the care to fully analyze the details, and till this day in his heart believes that I must be mistaken about most of these assumptions and conclusions.

It is sad to see, because to myself and to multiple friends, the issues seems obvious.

. . .

I would be very curious what you think of the deeper details outlined in the B-set, once you have had time to carefully read through and conclude your assessment of their contents.

Do you believe that all aspects of what is presented are plausible? If so, how can I strengthen support and recognition for their status? If not, when what details do you feel may be missing? If you were to play "Devil's advocate," where do you see weak spots or alternative explanations for what I see, obvserve, experience, hypothesize and report?

(On the matter of drugs remaining in the body at higher concentrations--indeed: cocaine is one such known drug that, in higher accumulations within normally-elastic intestinal tissue, is well-known by its use to be associated with intestinal tears. Such tears have been experienced by me, as reported on extensively in various documents, yet no doctor believes it because I have (1) pain, (2) inflammation, and (3) immune response all effectively blocked--these three indicators are the ONLY indicators that doctors can use with normal population to determine acute abdomen.

On the matter of drug detox protocols: yes, besides an actual hemoperfusion-type or M.A.R.S.-type set-up, the only other way is to use saunas, often with high-dose niacin, as recomended by a well-known MD (urologist and surgeon) within the detox community, Dr XXXXXXX Yu. This tactic works on people who have almost an type of toxin with does not directly neurologically interfere with the metabolic/excretory system functions, vis-a-vis the CNS. But in my case, past use of saunas and niacin have caused such massive releases of Phenibut/Fasoracetam drug, and effects, that the net progress is aactually negative, as the liver becomes more slowed as a result of the stronger circulatory presence and redistribution of fat-stored drug.)

Thank you for your dedication doctor. Your support means a lot to me.