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PATM proved real by MeBO clinical studies
@ healthhealth24
Those that don’t believe PATM is real, please watch video below of researchers’ initial finding for PATM, TMAU2 and Halitosis vs a Control Group. Someone posted it here and I just watched it for last hour. Researchers have found that PATM is real. They have also confirmed some of our findings on Restore and Brown Rice Powder and gut permeability (leaky gut). There are other findings but a little too technical to explain but you can watch it for yourself. So please forget about the whole delusional discussion and enlighten those that have been misguided for the past years. That would be very helpful for all of our community members. Please. I have posted on our current understanding of PATM and possible solutions on the main PATM forum. Please go read and comment. Thanks.
https://www.youtube.com/watch?v=ZBo6rzhVjl0&feature=youtu.be
Those that don’t believe PATM is real, please watch video below of researchers’ initial finding for PATM, TMAU2 and Halitosis vs a Control Group. Someone posted it here and I just watched it for last hour. Researchers have found that PATM is real. They have also confirmed some of our findings on Restore and Brown Rice Powder and gut permeability (leaky gut). There are other findings but a little too technical to explain but you can watch it for yourself. So please forget about the whole delusional discussion and enlighten those that have been misguided for the past years. That would be very helpful for all of our community members. Please. I have posted on our current understanding of PATM and possible solutions on the main PATM forum. Please go read and comment. Thanks.
https://www.youtube.com/watch?v=ZBo6rzhVjl0&feature=youtu.be
Hi guys.I think that PATM is electrosensitivity.I thought I had candida overgrowth due to antibiotics.But I don't have candida.I was diagnosed by bioresonance that I have mycotoxins in my guts -aflatoxin and aspergillus niger.There was black mold in my house due to antibiotics.Read about toxic mold illness which is enviromental disease.I also had 2 parasites-strongyloides and coronavirus.Coronavirus is a cat's parasite.I saw it in my stool.Now I'm on anti parasite program and antibiotic detox.Bioresonance say that everything has its own frequency.All of that crap -candida,mycotoxins,black mold,parasites feed on electromagnetic waves-smartphones,laptop etc.That's why detox is the most important.Also electromagnetic pulse helps about our situation.The woman tested what is good for me.Sacharomyces boulardii is not good for me because I don't have candida,Candida support also-it contains Pau dárco which is not good for me.Brown rice protein powder also is not ok for me.What works for me-Oxy powder because my main problem is in the guts,Digestive enzymes,coenzyme Q10,probiotic Lactacare daily which contains more bifido bacteria which is good for the colon and Raw Kombucha.It's all individual.It depends which pathogens a person has in the body.
6 Comments
@mindspace
At first when I saw posts about electromagnetism I used to think they are trolls trying to bring down the integrity of this forum. Sorry for mentioning this but it is factual and for some strange reason even now I’m still not sure if that’s the case or not.
Regardless here are facts, from a scientific point of view electromagnetism or whatever you’re talking about is simply impossible. The clinical studies also infer that it’s only a gas. I’m not sure if you understand anything about mass spectroscopy but it’s a process where compounds are ionized before separated. It’s the use of their small electrical charges to determine their masses. If PATM had anything to do electromagnetism this procedure and many others that are electromagnetic sensitive would not only fall apart but probably burn those instruments and perhaps scientists involved. Chemistry revolves around the idea of charges between atoms and molecules. It cannot escape what you claim unnoticed. Therefore, again, your claim is within the realm of the impossibility.
The candida idea is simply an idea without proof. The gut has hundreds of microbes but why have people pointed candida specifically? Why? It’s because somebody came up with idea and everybody took it as gospel and fact. Many sufferers have tested for candida and gotten negative results so thinking people naturally should abolish the idea unless proven otherwise.
The data that we’ve collected so far tells us clearly PATM is just toxins. Not only that but it’s microbial toxins originating at the gut. This is why people whom have taken very strong antibiotics and antifungal observe no PATM or minimal. Body removes toxins via sweat glands a lot so it’s no coincident why people who exercise or do sauna or hot bath with EPSOM salt, observe a decline in PATM. They are literally removing and minimizing the excessive toxins from their bloodstream but the leaky gut is constantly pumping toxins to the blood.90% of toxins comes straight from the gut. The other is from internal cellular process and elsewhere in the body.
The clinical studies by MeOB only confirmed this idea because I’ve always wondered how the hell that amount of toxins got through our gut and worse overload the liver. Gut permeability supports the idea really well. Studies have shown that gut permeability allows toxins and microbes into the blood stream. It’s quite peculiar why our immunity system doesn’t respond to these invaders like all other immunity problems i.e. peanut allergies. It appears our immunity is suppressed so much.
If gut permeability is true, it also infers that nutrients and drugs can easily absorb through the body. It also infers that some of us will show symptoms of weak immunity. There are exceptions to this but I wouldn’t be surprised if some of us with very bad gut permeability experience getting drunk quickly initially than normal because alcohol seeps through gut so fast, and also quick results from drugs, medication and supplements. The exception is the liver. Everything must go through the liver. If your liver is really healthy then it might not show. The immunity part suggests that you’d get sick easily from cold or sometimes probiotics if overdosed, common ear infections or infection elsewhere in the body.
At first when I saw posts about electromagnetism I used to think they are trolls trying to bring down the integrity of this forum. Sorry for mentioning this but it is factual and for some strange reason even now I’m still not sure if that’s the case or not.
Regardless here are facts, from a scientific point of view electromagnetism or whatever you’re talking about is simply impossible. The clinical studies also infer that it’s only a gas. I’m not sure if you understand anything about mass spectroscopy but it’s a process where compounds are ionized before separated. It’s the use of their small electrical charges to determine their masses. If PATM had anything to do electromagnetism this procedure and many others that are electromagnetic sensitive would not only fall apart but probably burn those instruments and perhaps scientists involved. Chemistry revolves around the idea of charges between atoms and molecules. It cannot escape what you claim unnoticed. Therefore, again, your claim is within the realm of the impossibility.
The candida idea is simply an idea without proof. The gut has hundreds of microbes but why have people pointed candida specifically? Why? It’s because somebody came up with idea and everybody took it as gospel and fact. Many sufferers have tested for candida and gotten negative results so thinking people naturally should abolish the idea unless proven otherwise.
The data that we’ve collected so far tells us clearly PATM is just toxins. Not only that but it’s microbial toxins originating at the gut. This is why people whom have taken very strong antibiotics and antifungal observe no PATM or minimal. Body removes toxins via sweat glands a lot so it’s no coincident why people who exercise or do sauna or hot bath with EPSOM salt, observe a decline in PATM. They are literally removing and minimizing the excessive toxins from their bloodstream but the leaky gut is constantly pumping toxins to the blood.90% of toxins comes straight from the gut. The other is from internal cellular process and elsewhere in the body.
The clinical studies by MeOB only confirmed this idea because I’ve always wondered how the hell that amount of toxins got through our gut and worse overload the liver. Gut permeability supports the idea really well. Studies have shown that gut permeability allows toxins and microbes into the blood stream. It’s quite peculiar why our immunity system doesn’t respond to these invaders like all other immunity problems i.e. peanut allergies. It appears our immunity is suppressed so much.
If gut permeability is true, it also infers that nutrients and drugs can easily absorb through the body. It also infers that some of us will show symptoms of weak immunity. There are exceptions to this but I wouldn’t be surprised if some of us with very bad gut permeability experience getting drunk quickly initially than normal because alcohol seeps through gut so fast, and also quick results from drugs, medication and supplements. The exception is the liver. Everything must go through the liver. If your liver is really healthy then it might not show. The immunity part suggests that you’d get sick easily from cold or sometimes probiotics if overdosed, common ear infections or infection elsewhere in the body.
I'm very far away from trolling because you don't know my situation.It was extreme.After last antibiotic I had fecal smell without having gas.I had itching all over my body.My hair and beard were electrified.PATM symptoms were extremely coughs,itchiness and rub noses.Now I'm getting better and better.Very rarely somebody coughs around me and It's because I'm that kind of person who sees every little detail.My tongue gets white when I'm on the net-normally it's pink.I quit my last job because my colleague said here smell of cat ****.Now I know that I have cat's parasite.It's very simple.Parasites and mycotoxins are poisonous.Do you ever smell black mold-it's like poisonous mushrooms.I had it in my room.Next month I'm going to see therapist with these electric lamp with sound waves.It kills parasites and mycotoxins.However the lamp is not ok for people who have serious kidney problems.I don't have it.I know that's the cure because that's how mycotoxins and parasites are feeding.
One more thing-the woman said that after 2 generations there will be no such problems because of GMO products.GMO change our DNA.
We will be genetically mutated.She tested whether I had GMO parasites.I don't have it.
We will be genetically mutated.She tested whether I had GMO parasites.I don't have it.
@kmt6878
Great findings. Totally agree. Actually CoQ10 is among the best antioxidants out there. There’s actually a research out there where a university in Europe performed a test on 3000 food and supplements and listed the antioxidants quantity in each food type. You can find the list and put it in excel and rank them. Just buy the foods with maximum antioxidants. Many people with liver problems do this. But you’re right, it’s good gut repairing too. Great post! Thanks for that.
Great findings. Totally agree. Actually CoQ10 is among the best antioxidants out there. There’s actually a research out there where a university in Europe performed a test on 3000 food and supplements and listed the antioxidants quantity in each food type. You can find the list and put it in excel and rank them. Just buy the foods with maximum antioxidants. Many people with liver problems do this. But you’re right, it’s good gut repairing too. Great post! Thanks for that.
@mindspace
Hey mindspace, careful with the electric lamp and all. Please don’t hurt yourself. Take it easy and hope you get better.
Hey mindspace, careful with the electric lamp and all. Please don’t hurt yourself. Take it easy and hope you get better.
I agree about CoQ10 and also digestive enzymes.I don't know why but it works for me.So about the lamp the woman does not recommend it because of the radiation but one of the members here said that he was cured by this lamp.If that is the last chance I'll try it.
Man it's amazing how MeBO researchers use PEG 400 to profile gut permeability which divided out the different groups statistically. Just amazing.
10 Comments
Frankly I do hope that non-patmers in this forum whom have spent years harassing members and accusing them of delusional and losing their minds, would come to their senses and brave enough to apologize for the constant bullying and false accusations over these years. Many PATM or TMAU members have suffered and gotten extremely confused because of this injustice done by the propagandists. I hope asking for a simple apology to unhappy members isn’t too much.
I've been in contact with Monell Center for advancing the taste and smell in Pennsylvania, specifically with Dr. George Preti.
He diagnosed hundreds of people with a defective gene that causes the dreaded fishy smell that people with TMAU suffer from.
Here are his words:
"Regarding your comments about "PATM" I have diagnosed and seen, in-person, more than 100 people with various cases of trimethylaminuria (TMAU); some of them were very severe cases but neither me or my staff have never reported or felt any of the symptoms (coughing, sneezing, eye irritation, etc) you describe."
This tells me that PATM and TMAU are two different disorders. Anybody have any comments?
He diagnosed hundreds of people with a defective gene that causes the dreaded fishy smell that people with TMAU suffer from.
Here are his words:
"Regarding your comments about "PATM" I have diagnosed and seen, in-person, more than 100 people with various cases of trimethylaminuria (TMAU); some of them were very severe cases but neither me or my staff have never reported or felt any of the symptoms (coughing, sneezing, eye irritation, etc) you describe."
This tells me that PATM and TMAU are two different disorders. Anybody have any comments?
Ray2502 thank you for that piece of information. We can only guess whether they are the same thing, separate or overlapping at this point because we don’t have enough evidence either way. The findings from MeBO clinical research so far, as we’ve also seen, only isolated PATM and TMAU from the other groups and since it’s a preliminary report we don’t know for sure about that particular circumstance.
Here are the key points we know from the studies so far.
1. All volunteers with PATM and TMAU were clearly separated from other groups using gut permeability.
2. Both PATM and TMAU all had similar low metabolites, especially the amino acids.
3. PATMers ended up being grouped together with TMAU in terms of odor.
I did ask them to give me an average gut permeability of PATM and TMAU because it will give us some ideas where they lie but they haven’t respond and I doubt they will since it’s a video a few months ago. I think it’s too early to tell at this point so it’s anybody’s guess. Let’s hope the study will continue. Their biggest problem is funding. If there’s not enough funding and interests from people they’d likely quit. That’s how scientific research goes in the real world.
I think the happiest news from all this is PATM has been scientifically proven to TRUE. This also means that Olfactory Reference Syndrome (ORS) is simply BS from insecure psychologists who are afraid of losing their jobs in the 21st century. Somebody should troll them on social media because if they are brave enough to spread their lies then we should be strong enough to tell the truth.
Here are the key points we know from the studies so far.
1. All volunteers with PATM and TMAU were clearly separated from other groups using gut permeability.
2. Both PATM and TMAU all had similar low metabolites, especially the amino acids.
3. PATMers ended up being grouped together with TMAU in terms of odor.
I did ask them to give me an average gut permeability of PATM and TMAU because it will give us some ideas where they lie but they haven’t respond and I doubt they will since it’s a video a few months ago. I think it’s too early to tell at this point so it’s anybody’s guess. Let’s hope the study will continue. Their biggest problem is funding. If there’s not enough funding and interests from people they’d likely quit. That’s how scientific research goes in the real world.
I think the happiest news from all this is PATM has been scientifically proven to TRUE. This also means that Olfactory Reference Syndrome (ORS) is simply BS from insecure psychologists who are afraid of losing their jobs in the 21st century. Somebody should troll them on social media because if they are brave enough to spread their lies then we should be strong enough to tell the truth.
dontgiveuphope,
Please read the following.
There is still alote of questions to be answered but it looks like TMAU is a genetic disorder.
Potential New Causes for the Odor-Producing Disorder TMAU
Exome sequencing provides insight into diagnostic criteria for rare metabolic disorder
PHILADELPHIA (February 14, 2017) – Just before Rare Disease Day 2017, a study from the Monell Center and collaborating institutions provides new insight into the causes of trimethylaminura (TMAU), a genetically-transmitted metabolic disorder that leads to accumulation of a chemical that smells like rotting fish.
Although TMAU has been attributed solely to mutations in a single gene called FMO3, the new study combined sensory and genetic approaches to identify additional genes that may contribute to TMAU. The findings indicate that genetic testing to identify mutations in the FMO3 gene may not be sufficient to identify the underlying cause of all cases of TMAU.
TMAU is classified as a “rare disease,” meaning that it affects less than 200,000 people in the United States. However, its actual incidence remains uncertain, due in part to inconclusive diagnostic techniques.
“Our findings may bring some reassurance to people who report fish-like odor symptoms but do not have mutations in the FMO3 gene,” said Monell behavioral geneticist Danielle R. Reed, PhD, a senior author on the study.
The socially and psychologically distressing symptoms of TMAU result from the buildup of trimethylamine (TMA), a chemical compound produced naturally from many foods rich in the dietary constituent, choline. Such foods include eggs, certain legumes, wheat germ, saltwater fish and organ meats. TMA, which has a foul, fishy odor, normally is metabolized by the liver enzyme flavin-containing monooxygenase 3 (FMO3) into an odorless metabolite.
People with TMAU are unable to metabolize TMA, presumably due to defects in the underlying FMO3 gene that result in faulty instructions for making functional FMO3 enzymes. The TMA, along with its associated unpleasant odor, then accumulates and is excreted from the body in urine, sweat, saliva, and breath.
However, some people who report having the fish odor symptoms of TMAU do not have severely disruptive mutations in the FMO3 gene. This led the researchers to suspect that other genes may also contribute to the disorder.
In the new study, published online in the open access journal BMC Medical Genetics, the research team combined a gene sequencing technique known as exome analysis with sophisticated computer modeling to probe for additional TMAU-related genes.
The study compared sensory, metabolic and genetic data from ten individuals randomly selected from 130 subjects previously evaluated for TMAU at the Monell Center.
Each subject’s body odor was evaluated in the laboratory by a trained sensory panel before and after a metabolic test to measure production of TMA over 24 hours following ingestion of a set amount of choline.
Although the choline challenge test confirmed a diagnosis of TMAU by revealing a high level of urinary TMA in all 10 subjects, genetic analyses revealed that the FMO3 gene appeared to be normal in four of the 10. Additional analyses revealed defects in several other genes that could contribute to the inability to metabolize the odorous TMA.
“We now know that genes other than FMO3 may contribute to TMAU. These new genes may help us better understand the underlying biology of the disorder and perhaps even identify treatments,” said Reed.
TMAU’s odor symptoms may occur in irregular and seemingly unpredictable intervals. This makes the disease difficult to diagnose, as patients can appear to be odor-free when they consult a health professional.
This was evidenced in the current study. Although all of the subjects reported frequent fish-odor symptoms, none was judged by the sensory panel to have a fish-like odor at the time of the choline challenge.
Monell analytical organic chemist George Preti, PhD, also a senior author, commented on the diagnostic implications of the combined findings, “Regardless of either the patient’s current sensory presentation or FMO3 genetics, the choline challenge test will confirm the TMA accumulation that reveals the presence of the disorder.”
Moving forward, the researchers would like to repeat the genetic analyses in a larger cohort of TMAU patients without FMO3 mutations to confirm which other genes are involved in the disorder.
“Such information may identify additional odorants produced by TMAU-positive patients, and inform the future development of gene-based therapies” said Preti.
Also contributing to the research were co-lead author Liang-Dar Hwang, Jason Eades, Chung Wen Yu, Corrine Mansfield, Alexis Burdick-Will, and Fujiko Duke of Monell; co-lead author Yiran Guo, Xiao Chang, Brendan Keating, and Hakon Hakonarson of the Center for Applied Genomics at the Children’s Hospital of Philadelphia; co-lead author Jiankang Li, Yulan Chen, and Jianguo Zhang of BGI-Shenzhen (China); Steven Fakharzadeh of the Perelman School of Medicine, University of Pennsylvania; Paul Fennessey of the University of Colorado Health Sciences Center; and Hui Jiang of BGI-Shenzhen, the Shenzhen Key Laboratory of Genomics, and the Guangdong Enterprise Key Laboratory of Human Disease Genomics.
Funding for the research was provided by the National Organization of Rare Diseases; National Institute on Deafness and Other Communication of the National Institutes of Health; Shenzhen Municipal Government of China; Shenzhen Key Laboratory of Genomics; and Guangdong Enterprise Key Laboratory of Human Disease Genomics. Philanthropic funding was provided by the TMAU Foundation, Volatile Analysis, Inc., the family of Mr. and Mrs. Richard Hasselbusch with matching funds from Merck Easy Match, and the late Ms. Bonnie Hunt.
Please read the following.
There is still alote of questions to be answered but it looks like TMAU is a genetic disorder.
Potential New Causes for the Odor-Producing Disorder TMAU
Exome sequencing provides insight into diagnostic criteria for rare metabolic disorder
PHILADELPHIA (February 14, 2017) – Just before Rare Disease Day 2017, a study from the Monell Center and collaborating institutions provides new insight into the causes of trimethylaminura (TMAU), a genetically-transmitted metabolic disorder that leads to accumulation of a chemical that smells like rotting fish.
Although TMAU has been attributed solely to mutations in a single gene called FMO3, the new study combined sensory and genetic approaches to identify additional genes that may contribute to TMAU. The findings indicate that genetic testing to identify mutations in the FMO3 gene may not be sufficient to identify the underlying cause of all cases of TMAU.
TMAU is classified as a “rare disease,” meaning that it affects less than 200,000 people in the United States. However, its actual incidence remains uncertain, due in part to inconclusive diagnostic techniques.
“Our findings may bring some reassurance to people who report fish-like odor symptoms but do not have mutations in the FMO3 gene,” said Monell behavioral geneticist Danielle R. Reed, PhD, a senior author on the study.
The socially and psychologically distressing symptoms of TMAU result from the buildup of trimethylamine (TMA), a chemical compound produced naturally from many foods rich in the dietary constituent, choline. Such foods include eggs, certain legumes, wheat germ, saltwater fish and organ meats. TMA, which has a foul, fishy odor, normally is metabolized by the liver enzyme flavin-containing monooxygenase 3 (FMO3) into an odorless metabolite.
People with TMAU are unable to metabolize TMA, presumably due to defects in the underlying FMO3 gene that result in faulty instructions for making functional FMO3 enzymes. The TMA, along with its associated unpleasant odor, then accumulates and is excreted from the body in urine, sweat, saliva, and breath.
However, some people who report having the fish odor symptoms of TMAU do not have severely disruptive mutations in the FMO3 gene. This led the researchers to suspect that other genes may also contribute to the disorder.
In the new study, published online in the open access journal BMC Medical Genetics, the research team combined a gene sequencing technique known as exome analysis with sophisticated computer modeling to probe for additional TMAU-related genes.
The study compared sensory, metabolic and genetic data from ten individuals randomly selected from 130 subjects previously evaluated for TMAU at the Monell Center.
Each subject’s body odor was evaluated in the laboratory by a trained sensory panel before and after a metabolic test to measure production of TMA over 24 hours following ingestion of a set amount of choline.
Although the choline challenge test confirmed a diagnosis of TMAU by revealing a high level of urinary TMA in all 10 subjects, genetic analyses revealed that the FMO3 gene appeared to be normal in four of the 10. Additional analyses revealed defects in several other genes that could contribute to the inability to metabolize the odorous TMA.
“We now know that genes other than FMO3 may contribute to TMAU. These new genes may help us better understand the underlying biology of the disorder and perhaps even identify treatments,” said Reed.
TMAU’s odor symptoms may occur in irregular and seemingly unpredictable intervals. This makes the disease difficult to diagnose, as patients can appear to be odor-free when they consult a health professional.
This was evidenced in the current study. Although all of the subjects reported frequent fish-odor symptoms, none was judged by the sensory panel to have a fish-like odor at the time of the choline challenge.
Monell analytical organic chemist George Preti, PhD, also a senior author, commented on the diagnostic implications of the combined findings, “Regardless of either the patient’s current sensory presentation or FMO3 genetics, the choline challenge test will confirm the TMA accumulation that reveals the presence of the disorder.”
Moving forward, the researchers would like to repeat the genetic analyses in a larger cohort of TMAU patients without FMO3 mutations to confirm which other genes are involved in the disorder.
“Such information may identify additional odorants produced by TMAU-positive patients, and inform the future development of gene-based therapies” said Preti.
Also contributing to the research were co-lead author Liang-Dar Hwang, Jason Eades, Chung Wen Yu, Corrine Mansfield, Alexis Burdick-Will, and Fujiko Duke of Monell; co-lead author Yiran Guo, Xiao Chang, Brendan Keating, and Hakon Hakonarson of the Center for Applied Genomics at the Children’s Hospital of Philadelphia; co-lead author Jiankang Li, Yulan Chen, and Jianguo Zhang of BGI-Shenzhen (China); Steven Fakharzadeh of the Perelman School of Medicine, University of Pennsylvania; Paul Fennessey of the University of Colorado Health Sciences Center; and Hui Jiang of BGI-Shenzhen, the Shenzhen Key Laboratory of Genomics, and the Guangdong Enterprise Key Laboratory of Human Disease Genomics.
Funding for the research was provided by the National Organization of Rare Diseases; National Institute on Deafness and Other Communication of the National Institutes of Health; Shenzhen Municipal Government of China; Shenzhen Key Laboratory of Genomics; and Guangdong Enterprise Key Laboratory of Human Disease Genomics. Philanthropic funding was provided by the TMAU Foundation, Volatile Analysis, Inc., the family of Mr. and Mrs. Richard Hasselbusch with matching funds from Merck Easy Match, and the late Ms. Bonnie Hunt.
@ray2502
I think there’s some miscommunication here. There’s two types of TMAU if you didn’t know. Type 1 and Type 2. The subjects in the study are TMAU2 as the woman said. I know the definition by heart. TMAU type 1 is caused by a failed gene responsible for the FMO3 liver enzyme. The FMO3 enzyme is responsible for removing several toxins including the TMA compound which smells fishy. That’s what I can get out from the top my head but what’s important is the MeBO experiment wasn’t concerned with TMAU type 1.
TMAU2 is not genetic and scientists don’t have proof of what causes it. I referred to it with just the usually name TMAU with the assumption that many here know what I’m talking about. That’s reason why I mentioned TMAU and PATM have a lot in common because scientists don’t know the causation of TMAU2. Many suspect gut microbial imbalance as the cause but there’s no experimental evidence to confirm that. That is why some clinics tried curing TMAU2. There are clinics that try to heal TMAU1 but I don’t think procedure will work but you never know.
I think there’s some miscommunication here. There’s two types of TMAU if you didn’t know. Type 1 and Type 2. The subjects in the study are TMAU2 as the woman said. I know the definition by heart. TMAU type 1 is caused by a failed gene responsible for the FMO3 liver enzyme. The FMO3 enzyme is responsible for removing several toxins including the TMA compound which smells fishy. That’s what I can get out from the top my head but what’s important is the MeBO experiment wasn’t concerned with TMAU type 1.
TMAU2 is not genetic and scientists don’t have proof of what causes it. I referred to it with just the usually name TMAU with the assumption that many here know what I’m talking about. That’s reason why I mentioned TMAU and PATM have a lot in common because scientists don’t know the causation of TMAU2. Many suspect gut microbial imbalance as the cause but there’s no experimental evidence to confirm that. That is why some clinics tried curing TMAU2. There are clinics that try to heal TMAU1 but I don’t think procedure will work but you never know.
@ray2502
One other thing, the usually belief is that TMAU2 is caused by a mutation in the FMO3 gene. Some accused antibiotics or other potent chemicals for screwing the liver and causing the mutation of this enzyme. However the trial by Taymount clinic proved otherwise because the patients got cured although they didn’t report back long enough to verify whether it’s permanent or not.
One other thing, the usually belief is that TMAU2 is caused by a mutation in the FMO3 gene. Some accused antibiotics or other potent chemicals for screwing the liver and causing the mutation of this enzyme. However the trial by Taymount clinic proved otherwise because the patients got cured although they didn’t report back long enough to verify whether it’s permanent or not.
@ray2502
Here’s another thing you’d be surprised about. Most clinics only know if a patient is type 1 or type 2 by asking them…lol. If you’ve always had it, it’s labelled type 1. If you’ve recently had it, it’s type 2. While it’s easy to test for TMA by doing a ratio of TMA against its oxidized version, it’s not as easy as checking for the FMO3 gene. I know this because I’ve done it couple of times. The DNA extraction process can take you a whole day but modern tools can help to quicken that process, after some preliminary preparation of chopping out those particular sequences then multiply via PCR, you have to use gel electrophoresis which will eat your time especially if you doing manual measurement. If you using a modern machine, then it will be quick. If doing manually it goings take a couple of hours or days. Automatic machinery has changed all that. I know that many here think that clinics would actually test for them…lol Not even unless it’s needed. So when you people go for a TMAU test, they’re only checking TMA proportion in their urine before and after given a high meal of choline/Carnitine rich food.
Here’s another thing you’d be surprised about. Most clinics only know if a patient is type 1 or type 2 by asking them…lol. If you’ve always had it, it’s labelled type 1. If you’ve recently had it, it’s type 2. While it’s easy to test for TMA by doing a ratio of TMA against its oxidized version, it’s not as easy as checking for the FMO3 gene. I know this because I’ve done it couple of times. The DNA extraction process can take you a whole day but modern tools can help to quicken that process, after some preliminary preparation of chopping out those particular sequences then multiply via PCR, you have to use gel electrophoresis which will eat your time especially if you doing manual measurement. If you using a modern machine, then it will be quick. If doing manually it goings take a couple of hours or days. Automatic machinery has changed all that. I know that many here think that clinics would actually test for them…lol Not even unless it’s needed. So when you people go for a TMAU test, they’re only checking TMA proportion in their urine before and after given a high meal of choline/Carnitine rich food.
dontgiveuphope,
Please don't take this in a bad way but these specialists at this Monel center have all the latest equipment years of expertise and I believe they are the one's who discovered the FM03 defective gene or have the most knowledge with TMAU. Did you see how many doctors, specialists and scientists contributed to the research that I posted above.
Anyways, I sent Dr. Peti an email concerning the different types of TMAU and here is his response.
"You appear to have been reading a lot of internet B.S.: you either have a form of TMAU or you do not. There are many genetic variants. Please read the material and description of Trimethylaminuria on our website.
If you wish to be tested for TMAU we perform the choline challenge test which reveals the presence of any variants."
Sincerely, George Preti
So my argument is that people that have TMAU don't necessarily have PATM and vice versa.
I have PATM but I'm almost 100% sure that I do not have TMAU. It has not been proven scientifically but I do not exhibit any of the symptoms of TMAU people.
PATM could be a defective gene of some type but we just don't know right now.
Please don't take this in a bad way but these specialists at this Monel center have all the latest equipment years of expertise and I believe they are the one's who discovered the FM03 defective gene or have the most knowledge with TMAU. Did you see how many doctors, specialists and scientists contributed to the research that I posted above.
Anyways, I sent Dr. Peti an email concerning the different types of TMAU and here is his response.
"You appear to have been reading a lot of internet B.S.: you either have a form of TMAU or you do not. There are many genetic variants. Please read the material and description of Trimethylaminuria on our website.
If you wish to be tested for TMAU we perform the choline challenge test which reveals the presence of any variants."
Sincerely, George Preti
So my argument is that people that have TMAU don't necessarily have PATM and vice versa.
I have PATM but I'm almost 100% sure that I do not have TMAU. It has not been proven scientifically but I do not exhibit any of the symptoms of TMAU people.
PATM could be a defective gene of some type but we just don't know right now.
@ray2502
LOL... no worries I understand you but I think you don't understand me. Don’t worry Ray, I think you will after this. It’s a tricky subject anyway. If you still don’t understand after this bro, I’ll take it down in details next Tuesday as I have something coming up that I have to attend.
This about this. What would you call a person with a faulty FMO3 gene and with high TMA in the blood? Second, what would you call a person with high TMA in the blood who doesn’t have the FMO3 mutated gene? If you can agree on the difference, then we can move on the next stage. The naming is a different issue but we should agree they are different.
If you’re talking about the different alleles for the FMO3 gene, then of course that’s a different matter altogether. A gene is nothing but a block of base pairs and could mutate in whatever way it could. Whatever protein or enzyme that translates out it is anybody’s guess depending on the sequence of amino acids. Some say there’s a new variant of the FMO3 gene identified every year.
Primary and Secondary TMAU is not about that. Primary and secondary TMAU is about whether you have a mutated gene or not. What I assume is that the chemist doesn’t know there are people who never had TMA elevation but got it later in life, and that those people have been given a specific name for their TMAU version.
The area of epidemiology is not for chemists, it’s for biologists, but the wise thing to always do is look up research papers first instead of asking someone because nobody has read all the biology papers on earth to keep track of everything even if he had all day…papers get published faster than anyone can read. The guy you asked is a chemist but not a biologist and I don’t think they were the one that discovered the mutated version of FMO3. If I remember correctly since I read this years ago it was discovered in the UK.
Ellie James is a type 2 or secondary TMAU patient. There’s many interviews on YouTube where her doctors who are specialists in TMAU, refer to her as a type 2. Ellie James has been interviewed explaining this too. Her doctor is among the expert in the UK on TMAU.
In the MeBO clinical research, they refer to the TMAU patient as TMAU2. Wikipedia also recognizes this. If you punch “Secondary TMAU” into google it gives you the meaning right away and unlimited links on the subject. If you type it into google scholar for peer reviewed papers, you’ll be drowned in papers mentioned TMAU2/Secondary TMAU. The papers mentioning Secondary TMAU or TMAU2 probably will take George Preti his whole lifetime to read and still not come half way to finishing it. Here’s the first few if you punch it down google school or a university peer reviewed journal database.
http://onlinelibrary.wiley.com/doi/10.1111/j.1440-1754.2010.01978.x/full
https://link.springer.com/chapter/10.1007/8904_2013_238
http://www.sciencedirect.com/science/article/pii/S0003986107002032
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3052392/
So are all scientists & people around the world all wrong except Geroge Preti? That’s very unlikely. What I assume is missing is that you’re pasting only parts of George’s email while he was actually referring to different alleles. If my assumption is right, then he’s correct too. This would mean we are just talking about two different things.
Btw, I’m not sure why they are testing for choline in the blood? Honestly if that’s some kind of new TMAU test then I’m not aware of it. I aware of eating rich choline food but testing for it in the blood doesn’t make any sense. I’ll look for papers on the subject time.
PATM a defective gene? Yes, you’re right…. it is possible. I’m hoping MeBO research can continue so we can get there. My guess is, if it’s the case, it would be a gene affecting epithelial cells. I use to think it’s a faulty enzyme in the liver but recent findings of MeBO wouldn’t explain the leaky gut.
LOL... no worries I understand you but I think you don't understand me. Don’t worry Ray, I think you will after this. It’s a tricky subject anyway. If you still don’t understand after this bro, I’ll take it down in details next Tuesday as I have something coming up that I have to attend.
This about this. What would you call a person with a faulty FMO3 gene and with high TMA in the blood? Second, what would you call a person with high TMA in the blood who doesn’t have the FMO3 mutated gene? If you can agree on the difference, then we can move on the next stage. The naming is a different issue but we should agree they are different.
If you’re talking about the different alleles for the FMO3 gene, then of course that’s a different matter altogether. A gene is nothing but a block of base pairs and could mutate in whatever way it could. Whatever protein or enzyme that translates out it is anybody’s guess depending on the sequence of amino acids. Some say there’s a new variant of the FMO3 gene identified every year.
Primary and Secondary TMAU is not about that. Primary and secondary TMAU is about whether you have a mutated gene or not. What I assume is that the chemist doesn’t know there are people who never had TMA elevation but got it later in life, and that those people have been given a specific name for their TMAU version.
The area of epidemiology is not for chemists, it’s for biologists, but the wise thing to always do is look up research papers first instead of asking someone because nobody has read all the biology papers on earth to keep track of everything even if he had all day…papers get published faster than anyone can read. The guy you asked is a chemist but not a biologist and I don’t think they were the one that discovered the mutated version of FMO3. If I remember correctly since I read this years ago it was discovered in the UK.
Ellie James is a type 2 or secondary TMAU patient. There’s many interviews on YouTube where her doctors who are specialists in TMAU, refer to her as a type 2. Ellie James has been interviewed explaining this too. Her doctor is among the expert in the UK on TMAU.
In the MeBO clinical research, they refer to the TMAU patient as TMAU2. Wikipedia also recognizes this. If you punch “Secondary TMAU” into google it gives you the meaning right away and unlimited links on the subject. If you type it into google scholar for peer reviewed papers, you’ll be drowned in papers mentioned TMAU2/Secondary TMAU. The papers mentioning Secondary TMAU or TMAU2 probably will take George Preti his whole lifetime to read and still not come half way to finishing it. Here’s the first few if you punch it down google school or a university peer reviewed journal database.
http://onlinelibrary.wiley.com/doi/10.1111/j.1440-1754.2010.01978.x/full
https://link.springer.com/chapter/10.1007/8904_2013_238
http://www.sciencedirect.com/science/article/pii/S0003986107002032
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3052392/
So are all scientists & people around the world all wrong except Geroge Preti? That’s very unlikely. What I assume is missing is that you’re pasting only parts of George’s email while he was actually referring to different alleles. If my assumption is right, then he’s correct too. This would mean we are just talking about two different things.
Btw, I’m not sure why they are testing for choline in the blood? Honestly if that’s some kind of new TMAU test then I’m not aware of it. I aware of eating rich choline food but testing for it in the blood doesn’t make any sense. I’ll look for papers on the subject time.
PATM a defective gene? Yes, you’re right…. it is possible. I’m hoping MeBO research can continue so we can get there. My guess is, if it’s the case, it would be a gene affecting epithelial cells. I use to think it’s a faulty enzyme in the liver but recent findings of MeBO wouldn’t explain the leaky gut.
@ray2502
Did you read my first post? I should get you the pdf so you can read it yourself. It’s a correspondence between an endocrinologist and TMAU2 person. The doctor explained how he cured a TMAU2 patient and was working on a second patient.
According to the doctor, the patient had to go out into coffee shops and get cozy with other people in trains to believe her odor is gone. She went back and reported her odor is gone and was cured. My question is, if it’s really an odor wouldn’t the doctor know? It would seem to me the doctor was just following his patient’s judgement. That seems to me to be a PATM patient who is confused. Most PATM here believe they have odors too.
If that’s case, then FMT can cure PATM if done properly by specialists. I think the poop pill is the best since it can work its way from the very top part of the intestine all the way down.
I wrote the clinic and they said the trial had to be abandoned because they lost contact with the patient so they can’t know for sure what’s the long term effect.
Did you read my first post? I should get you the pdf so you can read it yourself. It’s a correspondence between an endocrinologist and TMAU2 person. The doctor explained how he cured a TMAU2 patient and was working on a second patient.
According to the doctor, the patient had to go out into coffee shops and get cozy with other people in trains to believe her odor is gone. She went back and reported her odor is gone and was cured. My question is, if it’s really an odor wouldn’t the doctor know? It would seem to me the doctor was just following his patient’s judgement. That seems to me to be a PATM patient who is confused. Most PATM here believe they have odors too.
If that’s case, then FMT can cure PATM if done properly by specialists. I think the poop pill is the best since it can work its way from the very top part of the intestine all the way down.
I wrote the clinic and they said the trial had to be abandoned because they lost contact with the patient so they can’t know for sure what’s the long term effect.
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