You all helped save my life.
- Thread starter Shua1991
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Shua1991
Really Active Member
Coprine mushrooms can be farmed organically, they already appear in nature after seasonal rainfall. I will collect these spores as an agent within my environment, an "activated" genotype aka phenotype within my local ecology/surroundings.
I will help others forn the rest of my life.
As long as I live, as long as this heart still beats.
I will help others forn the rest of my life.
As long as I live, as long as this heart still beats.
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Shua1991
Really Active Member
CoprineCoprine (1-cyclopropanol-1-N5-glutamine) is a compound produced by edible mushrooms of the genus Coprinopsis (e.g., C. atramentaria, the death cap, the ink cap) that on ingestion causes a marked ethanol sensitivity.
From: Progress in Molecular Biology and Translational Science, 2012
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Mushrooms, Coprine
T.R. Peredy, in Encyclopedia of Toxicology (Third Edition), 2014
Background
Coprine-containing mushrooms such as Coprinopsis atramentaria, also known as the common inky cap mushroom is found in Europe and North America. It is a common fungus and arises often after rain showers throughout the northern hemisphere in the spring through autumn. It is edible; however, poisonous when consumed with alcohol – which is the source of one of the common names for this mushroom – tippler's bane.
Coprine has been isolated from C. atramentaria formerly Coprinus atramentarius; however, other Coprinus species such as the common edible Coprinus comatus (Shaggy Mane, Lawyer's wig) do not contain coprine. Other mushroom species are known to cause alcohol intolerance: Verpa bohemica, Clitocybe clavipes, Pholiota squarrosa, Tricholoma flavovirens, Mochella angusticeps, and Lepiota aspera, however, their mechanism of toxicity is unknown.
Toxicology and Human Environments
Ernest Hodgson, in Progress in Molecular Biology and Translational Science, 2012
2.3.5 Coprine
Coprine (1-cyclopropanol-1-N5-glutamine) is a compound produced by edible mushrooms of the genus Coprinopsis (e.g., C. atramentaria, the death cap, the ink cap) that on ingestion causes a marked ethanol sensitivity. The mechanism appears to be inhibition of the low Km form of liver acetaldehyde dehydrogenase by the active metabolite cyclopropanone hydrate. Although the overall effect resembles that of disulfiram, coprine (Fig. 14.1) does not affect dopamine-β-decarboxylase and is a more potent ethanol-sensitizing agent.2,15
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Hazards and Diseases
D. Clarke, C. Crews, in Encyclopedia of Food Safety, 2014
Antabuse Syndrome
Occurrence
It is caused by the fungi Coprinus atramentarius, Clitocybe clavipes, other Coprinus spp.
Toxicity
Coprinus species produce the compound coprine. This is not itself a poison but interferes with the alcohol detoxification process by inhibiting one of the enzymes (alcohol dehydrogenase) that processes alcohol. Alcohol is then broken down only partially to acetaldehyde. The symptoms of coprine poisoning are due to the build-up of acetaldehyde in the blood. Incidentally, the alcohol antabuse treatment disulfiram operates in the same manner, hence the syndrome being named ‘antabuse.’
Clinical Manifestations
Symptoms may occur shortly after the consumption of both the fungus and an alcoholic beverage up to 48 h after the fungi is eaten. Symptoms include a flushing of the face and neck, a metallic taste in the mouth, tingling of the extremities, rapid heartbeat, and a feeling of swelling in the face and hands. The initial symptoms may be followed by nausea and vomiting. Occasionally visual disturbances, vertigo, weakness, and confusion occur.
Diagnosis and Treatment
The symptoms will subside on their own in time, although the patient may be convinced that he or she has been seriously poisoned. Coprine poisoning is unpleasant but will run its course in a couple of hours without treatment. Coprinus atramentarius is edible and safe if cooked and if no alcohol is ingested within 2–3 days of eating the fungi.
Shua1991
Really Active Member
Mushrooms
David Spoerke MS, RPh, in Small Animal Toxicology (Second Edition), 2006
Coprine: rare
Coprinus atramentarius, C. micaceus, C. insignis, and Clitocybe clavipes are suspected of containing the toxin coprine. Clinical signs are exhibited shortly after the patient ingests an alcohol-containing product and the mushroom. For significant effects to occur, a coprine-containing mushroom should have been eaten within the last 24 to 72 hours. Ingested alone, without an alcohol product, these mushrooms are not toxic to humans. Ingestion of alcohol is unlikely in animals (barring fermenting fruit), so a human type of toxicity with this group of mushrooms is unlikely. The timing of the ingestion may be crucial. The clinical signs mimic those of the Antabuse (disulfiram)-alcohol interaction. Substances in these mushrooms have caused severe testicular injuries in dogs and rats.
Intravenous 4-methylpyrazole, administered at a dose of 5 mg/kg to humans, is known to terminate disulfiram-alcohol reactions and in theory terminates coprine reactions as well.89 This chemical inhibits alcohol dehydrogenase and therefore decreases acetaldehyde formation. It has not been tested for this use in animals, and is not a labeled indication for the drug.
David Spoerke MS, RPh, in Small Animal Toxicology (Second Edition), 2006
Coprine: rare
Coprinus atramentarius, C. micaceus, C. insignis, and Clitocybe clavipes are suspected of containing the toxin coprine. Clinical signs are exhibited shortly after the patient ingests an alcohol-containing product and the mushroom. For significant effects to occur, a coprine-containing mushroom should have been eaten within the last 24 to 72 hours. Ingested alone, without an alcohol product, these mushrooms are not toxic to humans. Ingestion of alcohol is unlikely in animals (barring fermenting fruit), so a human type of toxicity with this group of mushrooms is unlikely. The timing of the ingestion may be crucial. The clinical signs mimic those of the Antabuse (disulfiram)-alcohol interaction. Substances in these mushrooms have caused severe testicular injuries in dogs and rats.
Intravenous 4-methylpyrazole, administered at a dose of 5 mg/kg to humans, is known to terminate disulfiram-alcohol reactions and in theory terminates coprine reactions as well.89 This chemical inhibits alcohol dehydrogenase and therefore decreases acetaldehyde formation. It has not been tested for this use in animals, and is not a labeled indication for the drug.
Shua1991
Really Active Member
Pt 2. Continued
Mushrooms, Coprine
Anthony S. Manoguerra, in Encyclopedia of Toxicology (Second Edition), 2005
Mechanism of Toxicity
Poisoning with mushrooms in this group occurs when ethanol is consumed shortly before or within 5 days after eating the mushrooms. Coprine (N(5)-(1-hydroxy cyclopropyl)-l-glutamine) is the active constituent in these mushrooms and has been shown to inhibit liver aldehyde dehydrogenase. The active metabolite, cyclopropanone hydrate, has also been shown to possess similar activity. This inhibition of ethanol metabolism at the point of aldehyde dehydrogenase results in accumulation of acetaldehyde. In the absence of concurrent ethanol consumption, these mushrooms are edible.
"In the absence of cannabis compounds aka thiols/terpenes and mercaptans produced via Cannabis Sativa aka "catpiss phenotype" aka ammonia pheno"
No reactions were detected. No mechanism of action? I think not
it's plain as day if you have ameobas or "Borellia burgdorferi"(lyme disease bacteria living in my brain).
I do, and I can prove it via blood tests and spinal tissue samples or the urine samples containing their metabolic remains/detoxification.
Mushrooms, Coprine
Anthony S. Manoguerra, in Encyclopedia of Toxicology (Second Edition), 2005
Mechanism of Toxicity
Poisoning with mushrooms in this group occurs when ethanol is consumed shortly before or within 5 days after eating the mushrooms. Coprine (N(5)-(1-hydroxy cyclopropyl)-l-glutamine) is the active constituent in these mushrooms and has been shown to inhibit liver aldehyde dehydrogenase. The active metabolite, cyclopropanone hydrate, has also been shown to possess similar activity. This inhibition of ethanol metabolism at the point of aldehyde dehydrogenase results in accumulation of acetaldehyde. In the absence of concurrent ethanol consumption, these mushrooms are edible.
"In the absence of cannabis compounds aka thiols/terpenes and mercaptans produced via Cannabis Sativa aka "catpiss phenotype" aka ammonia pheno"
No reactions were detected. No mechanism of action? I think not
it's plain as day if you have ameobas or "Borellia burgdorferi"(lyme disease bacteria living in my brain).I do, and I can prove it via blood tests and spinal tissue samples or the urine samples containing their metabolic remains/detoxification.
Shua1991
Really Active Member
Pt 3
Interactions with medicinal cannabis aka
Terpene rich- thiol rich cannabis.
The kinds I grow at home, the kinds you all showed me how to grow using organic methods, egg shells/compost/ kelp/alfalfa teas and growing with garden gypsum and lime(lol lime fighting lyme) along with, lactic acid bacteria, all available on this website
Fuck rollitup those fags couldn't handle the truth I beat the upside their fucking skulls with it.
Interactions with medicinal cannabis aka
Terpene rich- thiol rich cannabis.
The kinds I grow at home, the kinds you all showed me how to grow using organic methods, egg shells/compost/ kelp/alfalfa teas and growing with garden gypsum and lime(lol lime fighting lyme) along with, lactic acid bacteria, all available on this website
Fuck rollitup those fags couldn't handle the truth I beat the upside their fucking skulls with it.
Shua1991
Really Active Member
Poisonous Plants and Aquatic Animals
David A Warrell, ... Michael Eddleston, in Hunter's Tropical Medicine and Emerging Infectious Disease (Ninth Edition), 2013
Other Toxic Events Caused by Fungi
Antabuse Syndrome
Species and Mechanisms of Toxicity
An antabuse reaction may be provoked by Coprinus atramentarius and possibly other Coprinus spp., Clitocybe clavipes, and Boletus luridus. The toxic principle is the presence of coprin that blocks aldehyde dehydrogenase, explaining why ingestion of these mushrooms in combination with ethanol may result in a typical antabuse syndrome. This risk will last for almost a week post-ingestion.
Symptoms
Symptoms mimic those of an ethanol—disulfiram reaction(“antabuse syndrome”): flushing, sweating, nausea, headache, tachycardia, anxiety, and circulatory disturbances.
Treatment
If the patient is admitted early, activated charcoal and gastric lavage may be useful. Otherwise, treatment is symptomatic and supportive.
Paxillus Syndrome
This syndrome is caused by ingestion of the “roll-rim cap”, Paxillus involutus. This mushroom can cause problems in two ways. First, it contains thermo-labile, strongly irritating toxins that may cause severe gastroenteritis if the mushroom is not cooked properly. Second, there are antigenic agents in this mushroom that are not denatured by cooking, explaining why people may become sensitized if the fungus is eaten repeatedly. These people may react violently to subsequent meals containing this mushroom. Symptoms are severe gastroenteritis, dehydration, hemolysis and associated kidney failure. Treatment is symptomatic.
Bolded for clarity.
David A Warrell, ... Michael Eddleston, in Hunter's Tropical Medicine and Emerging Infectious Disease (Ninth Edition), 2013
Other Toxic Events Caused by Fungi
Antabuse Syndrome
Species and Mechanisms of Toxicity
An antabuse reaction may be provoked by Coprinus atramentarius and possibly other Coprinus spp., Clitocybe clavipes, and Boletus luridus. The toxic principle is the presence of coprin that blocks aldehyde dehydrogenase, explaining why ingestion of these mushrooms in combination with ethanol may result in a typical antabuse syndrome. This risk will last for almost a week post-ingestion.
Symptoms
Symptoms mimic those of an ethanol—disulfiram reaction(“antabuse syndrome”): flushing, sweating, nausea, headache, tachycardia, anxiety, and circulatory disturbances.
Treatment
If the patient is admitted early, activated charcoal and gastric lavage may be useful. Otherwise, treatment is symptomatic and supportive.
Paxillus Syndrome
This syndrome is caused by ingestion of the “roll-rim cap”, Paxillus involutus. This mushroom can cause problems in two ways. First, it contains thermo-labile, strongly irritating toxins that may cause severe gastroenteritis if the mushroom is not cooked properly. Second, there are antigenic agents in this mushroom that are not denatured by cooking, explaining why people may become sensitized if the fungus is eaten repeatedly. These people may react violently to subsequent meals containing this mushroom. Symptoms are severe gastroenteritis, dehydration, hemolysis and associated kidney failure. Treatment is symptomatic.
Bolded for clarity.
Shua1991
Really Active Member
Pt. 4 Continued
Recent studies and biochemical data of coprine/disulfiram.
Case Histories
P. Lindberg, in Comprehensive Medicinal Chemistry II, 2007
8.17.1 My Early Years in Chemistry
My father was a mechanical engineer but had a special passion for chemistry. He conveyed this interest to me with such enthusiasm that, by the age of 13, when I had my first chemistry lessons at school, I knew that I wanted to be a chemist. On completion of my first degree in chemical engineering at the University of Technology in Lund, Sweden, in 1969, I therefore continued my studies there as a graduate student in the Organic Chemistry Department. I still regard my thesis work on the toxic principle of the mushroom Coprinus atramentarius, supervised by Professor Börje Wickberg, as my most important piece of work, which set the tone for the rest of my career.
8.17.1.1 My Thesis Work
The goal of my thesis work was to isolate and identify the toxic principle of the gray inky cap mushroom C. atramentarius. It had been known for some time that this mushroom was edible and palatable, but if eaten along with alcohol it caused flushing, nausea, vomiting, palpitation, and increased blood pressure. Numerous scientific publications had appeared in the literature going back to the beginning of the twentieth century, describing attempts to isolate the active principle, but without success. Börje Wickberg therefore made it clear at the outset that this project might present a challenge for a graduate student. He was right. It took a year of hard work before I had any breakthrough on how to monitor the isolation work, which we believed to be a prerequisite for future success.
In my thesis1 you can find the following footnote: “In a more-or-less desperate experimental situation during present attempts to find the toxic principle, the author ate 300 g of boiled C. atramentarius and then, on the following day, took 20 cL of ethanol (40%), but no uncomfortable effects were experienced.” Luckily, however, I finally developed a test method in rats, in which per oral administration of mushroom extracts dissolved in water was followed by a large dose of alcohol 6 h later. If the extract contained the active compound, the rats developed a tremendous facial edema some 12 h later. Using this test method to monitor the success of extraction and separation techniques, I was able to isolate the active compound in a couple of months.1,2
Elucidation of the structure of the active compound was performed in the classical way, and various degradation reactions finally revealed N5-(1-hydroxycyclopropyl)-glutamine (coprine; 1), the first (and probably still the only) natural product to be isolated that contains a cyclopropanone equivalent. After initial synthesis of the important fragment, 1-hydroxycyclopropylammonium chloride (2) (the free base being unstable), from cyclopropanone, concentrated ammonia and concentrated hydrochloric acid, I was able to synthesize the compound via an efficient photolysis reaction. By acylation of 1-hydroxycyclopropylamine by means of N1-phthaloyl-glutamic acid anhydride, coprine could be synthesized in good yield.1,2
Bolded for clarity/importance
As it was thought that the reaction with the mushroom and concomitant alcohol was caused by inhibition of the liver aldehyde dehydrogenase, I began by testing mushroom extracts for their ability to inhibit the partially purified enzyme from bovine liver, but with no success. After fruitless attempts to establish an efficient collaboration with pharmacologists at the local university, I also introduced my own animal testing (in the chemistry laboratory) and started working with mice, again without success.
Recent studies and biochemical data of coprine/disulfiram.
Case Histories
P. Lindberg, in Comprehensive Medicinal Chemistry II, 2007
8.17.1 My Early Years in Chemistry
My father was a mechanical engineer but had a special passion for chemistry. He conveyed this interest to me with such enthusiasm that, by the age of 13, when I had my first chemistry lessons at school, I knew that I wanted to be a chemist. On completion of my first degree in chemical engineering at the University of Technology in Lund, Sweden, in 1969, I therefore continued my studies there as a graduate student in the Organic Chemistry Department. I still regard my thesis work on the toxic principle of the mushroom Coprinus atramentarius, supervised by Professor Börje Wickberg, as my most important piece of work, which set the tone for the rest of my career.
8.17.1.1 My Thesis Work
The goal of my thesis work was to isolate and identify the toxic principle of the gray inky cap mushroom C. atramentarius. It had been known for some time that this mushroom was edible and palatable, but if eaten along with alcohol it caused flushing, nausea, vomiting, palpitation, and increased blood pressure. Numerous scientific publications had appeared in the literature going back to the beginning of the twentieth century, describing attempts to isolate the active principle, but without success. Börje Wickberg therefore made it clear at the outset that this project might present a challenge for a graduate student. He was right. It took a year of hard work before I had any breakthrough on how to monitor the isolation work, which we believed to be a prerequisite for future success.
In my thesis1 you can find the following footnote: “In a more-or-less desperate experimental situation during present attempts to find the toxic principle, the author ate 300 g of boiled C. atramentarius and then, on the following day, took 20 cL of ethanol (40%), but no uncomfortable effects were experienced.” Luckily, however, I finally developed a test method in rats, in which per oral administration of mushroom extracts dissolved in water was followed by a large dose of alcohol 6 h later. If the extract contained the active compound, the rats developed a tremendous facial edema some 12 h later. Using this test method to monitor the success of extraction and separation techniques, I was able to isolate the active compound in a couple of months.1,2
Elucidation of the structure of the active compound was performed in the classical way, and various degradation reactions finally revealed N5-(1-hydroxycyclopropyl)-glutamine (coprine; 1), the first (and probably still the only) natural product to be isolated that contains a cyclopropanone equivalent. After initial synthesis of the important fragment, 1-hydroxycyclopropylammonium chloride (2) (the free base being unstable), from cyclopropanone, concentrated ammonia and concentrated hydrochloric acid, I was able to synthesize the compound via an efficient photolysis reaction. By acylation of 1-hydroxycyclopropylamine by means of N1-phthaloyl-glutamic acid anhydride, coprine could be synthesized in good yield.1,2
Bolded for clarity/importance
As it was thought that the reaction with the mushroom and concomitant alcohol was caused by inhibition of the liver aldehyde dehydrogenase, I began by testing mushroom extracts for their ability to inhibit the partially purified enzyme from bovine liver, but with no success. After fruitless attempts to establish an efficient collaboration with pharmacologists at the local university, I also introduced my own animal testing (in the chemistry laboratory) and started working with mice, again without success.
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Shua1991
Really Active Member
Pt.5 animals studies and data done overseas, where it could be studied freely(no federal bans on research, like embryos research)
8.17.1.2 My First Pharmaceutical Project
In 1974, Börje Wickberg and I, along with Professor Arvid Carlsson (Nobel Laureate in Medicine in 2000) of the Department of Pharmacology, University of Göteborg, established an industrial collaboration, supported by the Swedish Board for Technical Development (STU) and sponsored by the Swedish pharmaceutical companies Astra and Kabi, with the aim of developing a new alcoholic deterrent with fewer side effects than disulfiram (Antabuse, the alcoholic deterrent used most commonly at the time).3 An additional chemist, Rolf Bergman, was employed and worked under my supervision in this program. Our work focused on making analogs in a structure–activity relationship program and on the development of a large-scale synthetic pathway to the cyclopropanone moiety of coprine (i.e., compound 2) and hence to coprine itself, which we eventually synthesized in a 250 g scale for toxicity studies. Our effort was aided on the biochemical side through collaboration with Dr Olof Tottmar (and his graduate student Hans Marchner4: in 1979, Hans Marchner defended his thesis on the mode of action of coprine and 1-aminocyclopropanol) at the University of Uppsala. Tottmar was an expert on liver aldehyde dehydrogenase and inhibition of this enzyme by Antabuse and other chemicals.5
The pharmaceutical project was discontinued in 1977 due to the unacceptable chronic toxicity (testicular lesions) of coprine in both rats and dogs.6 C. atramentarius has since been considered as toxic in mushroom handbooks, leading one to speculate about how many edible and palatable mushrooms are chronically toxic without giving any acute symptoms.
8.17.1.2 My First Pharmaceutical Project
In 1974, Börje Wickberg and I, along with Professor Arvid Carlsson (Nobel Laureate in Medicine in 2000) of the Department of Pharmacology, University of Göteborg, established an industrial collaboration, supported by the Swedish Board for Technical Development (STU) and sponsored by the Swedish pharmaceutical companies Astra and Kabi, with the aim of developing a new alcoholic deterrent with fewer side effects than disulfiram (Antabuse, the alcoholic deterrent used most commonly at the time).3 An additional chemist, Rolf Bergman, was employed and worked under my supervision in this program. Our work focused on making analogs in a structure–activity relationship program and on the development of a large-scale synthetic pathway to the cyclopropanone moiety of coprine (i.e., compound 2) and hence to coprine itself, which we eventually synthesized in a 250 g scale for toxicity studies. Our effort was aided on the biochemical side through collaboration with Dr Olof Tottmar (and his graduate student Hans Marchner4: in 1979, Hans Marchner defended his thesis on the mode of action of coprine and 1-aminocyclopropanol) at the University of Uppsala. Tottmar was an expert on liver aldehyde dehydrogenase and inhibition of this enzyme by Antabuse and other chemicals.5
The pharmaceutical project was discontinued in 1977 due to the unacceptable chronic toxicity (testicular lesions) of coprine in both rats and dogs.6 C. atramentarius has since been considered as toxic in mushroom handbooks, leading one to speculate about how many edible and palatable mushrooms are chronically toxic without giving any acute symptoms.
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Shua1991
Really Active Member
As of now, this the most current research on the naturally occuring biochemically available drug "coprine" which mimics the very sulfur pills ive taken for six months this can all be digested by me now thanks to this compound, these sulfur pills have cleared my brain of a 5+ year fog. No more dementia, this compound also helps defend against what is killing bee colonies worldwide(similar pandemic) called "colony collapse disorder.
this disulfiram kills and fights the disease responsible for the bees colony in queens who spread "deformed wing virus". A disease responsible for preventing our farm crops from r ebounding every year, fewer harvests fewer food sources less bees, less food.
We all starve as a result.
this disulfiram kills and fights the disease responsible for the bees colony in queens who spread "deformed wing virus". A disease responsible for preventing our farm crops from r ebounding every year, fewer harvests fewer food sources less bees, less food.
We all starve as a result.
Shua1991
Really Active Member
Concepts necessary for understanding
1. Inflammation of Central nervous system/immune response caused by bacterial/viral contagion
2. Bee venom therapy in response to infectious pathogens/disease, lack of arthritis induced inflammatory response.
3. Currently available biomedical markers for infection
Without being able to test these on a scale large enough to provide a significant results, we are left with an invisible/2 invisible pandemics waiting to be acknowledged.
The time to act is now.
1. Inflammation of Central nervous system/immune response caused by bacterial/viral contagion
2. Bee venom therapy in response to infectious pathogens/disease, lack of arthritis induced inflammatory response.
3. Currently available biomedical markers for infection
Without being able to test these on a scale large enough to provide a significant results, we are left with an invisible/2 invisible pandemics waiting to be acknowledged.
The time to act is now.