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Avatar universal

Woman with formal diagnosed TMAU2, same symptoms with PATM but with an odor.

If you watch the documentary below, it’s a British lady with TMAU2. As she explained in her own words, if she’s in a train people will rub their noses, cough and sneeze because she’s literary gassing them. I’ve seen a video where her TMAU doctors think antibiotics may have screwed her liver enzymes. I’m assuming they mean the FMO3. Here’s the funny thing, there’s no way to tell if her enzyme is failing unless you take a sample of her liver. This is not easy to do without opening the body in some way. You can only test for TMA/TMAO concentration ratios on urine or blood samples. I’m not so sure if it’s appropriate to make an overarching conclusion with very limited tests. I’m starting to doubt whether she actually got tested for TMA or not because she said her odor smells like rubber. What if her odor was caused by a completely different compound other than TMA and failure of a different enzyme or perhaps the problem lies in the gut rather than liver? I really don’t know the details about her formal diagnosis but I’m curious.


Part below of the same video and I quote her, “I went to several GP and they didn’t know what I had but most suggested that I have a mental health problem and that I was imagining it”. It took her 11 years until real specialists helped her. Poor lady.

6 Responses
Avatar universal
I agree, she does not seem to be a TMAU, but rather a PATM patient to me. I know a few people with PATM who have similar odours, as described by her in the video, it does not look like she was ever tested for TMAU and the doctor that has "diagnosed" her seems to have pulled this diagnosis out of thin air.

This doctor is a GP, not a metabolism or any other kind of specialist AND he has been asked to provide with a diagnosis for the TV show - this show might be just as big of a thing for him as it is for her, so in the end he just wants to appear competent.

Why did they choose him and not some specialist is a good question, but what would any specialist say about her symptoms is even a better question. She says she makes people rub their noses, their eyes water, they cough, they sneeze! As we all know very well, in the eyes of 99.999% of doctors anyone with PATM has ever seen - that's just crazy talk. :) But hey - we got some mainstream TV exposure in English! I think that's a first!
Besides that there are people, even on this board, that have/had both PATM and TMAU. Soiledsystem got rid of his TMAU2, with antibiotics, but PATM stayed, so she might have both as well.
Yes, I agree. The difference is really hard to tell though. Even the MeBO researchers have not found a difference between the two yet... but they will I think.
Wow, found this at mebblog.com. It seems there is a way to test for TMAU2 on urine samples alone without looking for liver enzymes at all. I was wrong. I'm directly quoting from the webpage,

"Substrate overload of FMO3 enzyme activity resulting from either an excess of dietary precursors of TMA or variations in gut fauna, causing increased release of TMA. This type of trimethylaminuria is characterized by a high concentration of TMA in the urine, but a normal urinary TMA/TMA N-oxide ratio."

I didn’t know that, honestly. Sorry folks! So if she’s TMAU2 then she’s depicting both symptoms that we PATMers express but with an additional odor. Now what the hell would that mean?

Does she have one or two failed enzyme, or two overloaded substrates? This would imply an elevation of both TMA and something else from an unbalance gut flora? Or FMO3 enzyme which can oxidize about 1000 different kind of compounds is just failing or failing with another enzyme. Very confusing now!!
Or does she have body flora that screws up her enzymes, or produces too much TMA? I think for most people this is mostly a microbiological problem, not a genetic one, most likely due to overuse of antibiotics in the last few years.
Yeah, I think research will eventually uncover those parts. The real question is when. I like what MeBO is doing. The only problem with their research is the financial side. There aren't many sufferers or donors.
Avatar universal

Look at the following interview, this is exactly what I was trying to describe earlier in my post. Ray was trying to describe the same thing earlier, he believes it's most likely an enzyme deficiency. The last two sentences are important. The scientist is explaining that other conditions like TMAU may exist and it could be two possibilities 1) unusual gut flora 2) lack of a detoxifying enzyme (liver enzyme).

Ma Mr Nigel Manning, Principal Clinical Scientist
Dept. Clinical Chemistry

Many people, including people with primary or secondary TMAU diagnosis, as well as those who are negative, have wide ranging odors. From gas/fecal to rotten egg and all sorts. Do you have a theory on this ?

“Body odour is caused by the release of volatile compounds from the skin in sweat. Just as TMA is produced in the gut by bacteria, there are probably many other volatile compounds which are naturally produced – like skatole which has a faecal odour. Only when the production of these compounds are produced in excess that the odour can become a problem. There may be other conditions like TMAU which are caused by an unusual gut flora as well as a lack of a detoxifying enzyme. Unfortunately we only have the ability to test for TMA at the moment.”

Do you think with a TMAU diagnosis, they will only smell of 'fish body odor' ?

"It may be possible to be afflicted with overproduction of more than one volatile compound if conditions in the gut are such that excesses of different species of odour-causing bacteria are pre-dominant. Other bacteria may be responsible for a mixture of volatiles. Some species of Shewanella are known to produce both TMA and hydrogen sulphide (rotten egg gas)."
Do you think with a TMAU diagnosis, they will only smell of 'fish body odor' ?
I think that nothing is clear until it is verified, but yes, who knows what other compounds might be produced by enzyme deficiencies and different bacterial overgrowth. I also think that maybe TMA does not smell all that bad? Maybe it is some other component in TMAU patients that stinks badly? Need to read up on these things at some point, at the moment just don't have that much time.
“Do you think with a TMAU diagnosis, they will only smell of 'fish body odor' ?”

I get confused on this question a lot. The right answer is yes because TMAU, the acronym for Tri-methyl-aminuria, is referring to the tri-methyl-amine (TMA) compound, the fishy smelly substance. TMAU is always testing for the presence of TMA. If it’s a different compound it isn’t TMAU anymore but most are always thinking that TMAU means any body odor but it’s not. It’s a direct reference to the TMA smelly compound. I get confused because sometimes I mean in a general sense like everyone else and sometimes I’m referring to the strict technical meaning.

“I think that nothing is clear until it is verified, but yes, who knows what other compounds might be produced by enzyme deficiencies and different bacterial overgrowth.”

Agree. There’s just too much we don’t know. Time will tell.

“I also think that maybe TMA does not smell all that bad?”

TMA is just a single compound. It’s just a nitrogen atom connected to 3 methyl group. It’s always smelling like rotten fish all the time. The chemical structure determines it’s properties; fish smelling is one of its properties.

It is however possible that there are other stinking or non-stinking compound that FMO3 is incapable of oxidizing but was supposed to.

“Maybe it is some other component in TMAU patients that stinks badly? Need to read up on these things at some point, at the moment just don't have that much time.”

Yes, that’s very true. For me, I understand it but the everyday use of TMAU is very confusing sometimes. It’ is possible for TMAU to co-exist with other things. Perhaps FMO3 enzyme is struggling to oxidize several smelly compounds including TMA.
Avatar universal
Wow! Look at this. TMAU2 kid cured by antibiotics alone. I guess the kid had no resistance because he didn't use antibiotics before so it was easy to kill off the bad gut bacteria.

Secondary TMAU only seems to be tested in the UK that we know of. Why do you think this is so ?

"Secondary TMAU or TMAU2 has been recognized for many years, although much of the TMAU interest has been in the inherited metabolic disorder FMO3 deficiency ie TMAU1. Very early on in the TMA service I received a urine from a pre-school age boy who was very odorous after eating fish. This was especially problematic because fish fingers were his favourite food and his parents had to persuade the parents of his friends to not serve fish fingers at birthday parties. The prospect of this going on when he started school was worrying, but after finding out about TMAU the parents arranged for the test to be done here. When I saw the very high TMA and TMO I suggested to the GP that a short course of the antibiotic metronidazole might help. After this dose this 4 year old had no more problems and could enjoy fish and chips with his family with no resulting odour – and still does ten years on. His TMAU had been cured and it convinced me that TMAU2 was an important part of the differential diagnosis.
TMAU2 from overproduction of TMA by bacterial overgrowth can be experienced for many years but if the correct antibiotic therapy is applied, can be cured by eradication of the bacterial responsible. Testing for TMAU1 or 2 is essentially the same, but results can usually differentiate one from the other. As I mentioned before there have been several occasions when a patient with marked increases in both urinary TMA and TMA-oxide (a TMAU2 pattern) then tests positive for TMA but with normal TMA-oxide (a TMAU1 pattern). This is why the DNA follow-up is so important."

It's interesting because someone a few years ago on this forum and another person on another forum, claimed he was cured with metronidazole but sadly after months, he came and reported that it had come back.

I tried metronidazole myself and PATM disappeared but only for two weeks and then resistance.

I wish I had my hands on Teixobactin or the newest version of neomycin.
Avatar universal
MEBO recommends vitamin B supplement to maximize FM03 production. Second, activated charcoal - helping to remove toxins. They make activated charcoal derived from coconut which you can add to gluten-free banana breads, almond butter etc. Odorless TMAU is well documented in medical literature, its possible that we have this is some form.

Imo, you don't need a clinical lab test to see if have TMAU.  Yesterday I had Poke, Hawaiian/ Japanese food with tons of Tuna (high in foline) to see what would happen. My digestion is still wacky today. If your body responds adversely to high foline foods (broccoli, salt-water seafood, peanut butter) its likely TMAU is at least part of the PATM puzzle.

Someone on the TMAU forum said they have literal FMO3 enzymes you can buy from a lab in Europe. I'm not about to take these but its interesting to know something like this exists.

w w w.abcam.com/FMO3-antibody-ab62178.html
“MEBO recommends vitamin B supplement to maximize FM03 production.”

Yes, I have bottles of Vit. B2 lying everywhere. It’ll make you burn…not the thing to take in summer. It didn’t show anything for me personally but that’s OK because it’s meant for the FMO3 enzyme itself. It could be another enzyme. FMO3 will work for TMAU patients but what if it’s another enzyme for PATM, or perhaps 2 or more enzymes are actually failing. We don’t know so I agree it’s better to try and see if it works. It didn’t work for me.

“Second, activated charcoal - helping to remove toxins. They make activated charcoal derived from coconut which you can add to gluten-free banana breads, almond butter etc.”

Charcoal is good, I use tons of it all the time. It works only when I use it in large amounts. It’s known to work for TMAU but not so much for PATM.

“ Odorless TMAU is well documented in medical literature, its possible that we have this is some form.”

I was just explaining to @LaserShark8 the confusion part regarding this. The idea is simple but actual using of words in general and technical are different. In general people refer to TMAU as a disease of any body odor; I sometimes do that. But in a strict technical meaning, Tri-methyl-aminuria (TMAU) is actually referring to the odor disease caused by the tri-methyl-amine (TMA) smelly compound. So in actual sense, TMA, always smell fishy, just as methane always smell like the sewer. TMAU is always referring to elevated TMA concentration in the blood.

“Imo, you don't need a clinical lab test to see if have TMAU.  Yesterday I had Poke, Hawaiian/ Japanese food with tons of Tuna (high in foline) to see what would happen.”

I think what you mean is whether you have some kind of odor condition. I agree. Sometimes it’s easy to tell but we still need a test to verify exactly what it is so we can address the problem directly.

“Someone on the TMAU forum said they have literal FMO3 enzymes you can buy from a lab in Europe. I'm not about to take these but its interesting to know something like this exists.”

Interesting, but the real problem is not making the enzyme because a recombinant bacterium can easily do the job and mass produce. Insulin and many other hormones is made this way. The problem is getting it inside our body. FMO3 enzyme is always in our liver cells where detoxification is done. If we take artificial FMO3 enzyme orally, all protein is destroyed, broken down into simple amino-acids. Enzymes are specific proteins that combine stuff or break stuff. Once it gets into the stomach breaking of protein, including enzymes, starts all the way to the intestine. This breaking down of enzymes in food is also done by other enzymes. FMO3 enzyme will not survive throughout the gut. It will get broken down into amino acids.
But what if we have a different enzyme problem other than FMO3?

“w w w.abcam.com/FMO3-antibody-ab62178.html”

This is an anti-FMO3 antibody. Antibodies and enzymes are not the same thing. I believe it’s probably there to help in some way for TMAU patients but I need to read up how it does it. Surely it’s not doing any oxidation because it’s not an enzyme but perhaps it helps via an alternative chemical pathway in regards to immunity.
I'm still confused about what Dr. Preti @ the Monell Chemical senses center said and I quote him "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.  If you wish further information regarding getting tested for TMAU, please see our web site at www.monell.org

Sincerely, George Preti
If you read the following, the scientists did mention that the test subjects, even though complained about fishy smell, they did not present the smell during testing of TMAU.

"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."
Here is another pdf file with information about TMAU. I personally do not have any issues with any of the foods that they mention that are rich in choline except peanut butter, soy, and wheat germ.
Here is the pdf file on TMAU, please read.

Trimethylaminuria (TMAU), formerly known as “Fish-Odor Syndrome,” is a genetically-transmitted metabolic disorder that causes patients to give off an unpleasant body odor.
People with TMAU are missing or have a defect in the enzyme that allows them to completely metabolize (break down) trimethylamine (TMA), a chemical compound found naturally in many foods. TMA has a foul, fishy odor. At low concentrations, it may be perceived as unpleasant or “garbage-like.”
The principal symptoms of TMAU stem from accumulation of excess TMA – and its associated unpleasant odor – which is then excreted from the body in urine, sweat, saliva, and breath.
A spectrum of changes to the gene coding for the critical enzyme, known as flavin-containing monooxygenase enzyme 3 (FMO3), results in varied degrees of impairment of FMO3’s ability to metabolize TMA. Depending upon the specific type of gene mutation, the amount of unmetabolized TMA and the related odor varies from individual to individual. Only about 10-15% of patients with TMAU have an odor that can be characterized as “fishy.”
Excessive production of TMA is linked to the intake of choline-rich foods, including eggs; certain legumes such as soy, kidney beans, etc; wheat germ; saltwater fish; and organ meats, including liver. Importantly, TMA production and associated odor symptoms depend on what foods recently have been eaten and therefore may occur in irregular and seemingly unpredictable intervals. Because many foods contain choline, it usually is difficult for patients and their family members to make a connection between symptoms and food intake.
Symptoms may include foul body odors, halitosis (bad breath) and/or dysguesia (bad taste or mouth feel). These can produce social embarrassment. Often, symptoms can only be temporarily relieved by normal hygiene procedures. Further, the unpleasant symptoms are often sporadic in occurrence and seemingly subjective. These characteristics, combined with a lack of knowledge of the disease and its etiology among health professionals, often lead to misdiagnosis of poor hygiene, psychiatric problems and/or referrals to other specialists.
- continued -
Monell Chemical Senses Center
3500 Market St., Philadelphia, PA 19104 215.898.6666 www.monell.org
Consequently, a resulting and persistent problem afflicting most patients are psychosocial ones caused by sporadic, unexplained malodor production and by the unpleasant and unforgiving reactions of people in schools and the workplace. Several reports in the literature have described other complications occurring in conjunction with TMAU; these include seizure, skin rashes, sarcoidosis and Prader-Willi and Noonan’s syndromes. However, the majority of patients have normal mental and physical abilities, lead normal lives, and have good hygiene practices.
TMAU is diagnosed using a biochemical test that measures the amount of TMA in the urine following ingestion of 12-16 oz of juice containing 5 g of added choline. A definitive diagnosis often is reassuring to many patients. Currently there is no cure for TMAU. However, current treatment options, including avoidance of choline-containing foods, can help reduce odor production for those afflicted with the disorder.
@Ray2502, I agree it is confusing sometimes to all of us. Probably if we knew everything, we’d have solved it ourselves…lol. TMA itself is just a fishy odor compound – Nitrogen with tri methyl groups attached – there are no ifs about the uniqueness of this compound as we agree. But if this woman has TMAU2, meaning she had elevated TMA but stable TMA/TMO ratio then it appears what she’s describing, the allergies, could be an additional problem on top, if we are to stick to the strict definition of TMAU, regardless of TMAU1 or TMAU2.

Btw, Ellie James has said in her many interviews she has TMAU2 according to her doctors. This documentary was one of the earliest and wasn’t mentioned but she’s got tons of other interviews either on TV or web.

Ellie didn’t have the condition until in her early 30s, which precisely mean it’s not genetic. She continued to have the condition for 11 years after that, before it was formally diagnosed.

According to her doctors, not the clown doctors in the video below, they think cycles of antibiotics she took may have mutated her liver enzyme… I’m assuming they meant FMO3 but I can’t recall. The doctors were interviewed. I’m assuming they’re not sure whether it’s the FMO3 or maybe gut dysbiosis or something else altogether. She and her doctors had lots of interviews on this so you might want to look it up to see and judge for yourself. I can’t find audio versions on YouTube anymore.

I know it’s confusing but if it’s confusing for specialists, then surely it will happen to us. TMAU1 has been well laid out. We know everything about it. A few words can pretty much describe it all, a faulty FMO3 gene and enzyme, and everyone knows what comes after it.

But TMAU2, well it’s kinda murky. We only know patients didn’t have it genetically and that they produce TMA, and the rest, specialists don’t agree or don’t know yet. What caused it, we aren’t sure and neither do specialists.

For what she describing, I now think that maybe she has both TMAU2 and PATM, or maybe TMAU2 always comes with PATM but PATM doesn’t necessary accompany TMAU2.

The woman below, Karen, claims to have TMAU2 as well. I wrote her because I believe she may have been misdiagnosed, and PATM instead, and she told me that no one goes on TV without being formally diagnosed. At that time, I was skeptical but now I think maybe she’s right, TV station wouldn’t waste their time on self-diagnoses because it’s unprofessional journalism to do so. I don’t’ know her case in particular because I haven’t seen her doctors being interviewed; someone can always write her for more questions like I did. I grabbed her email from one of the TMAU forums I think, a couple of years back, and had some correspondence with her.

There was another woman almost with the same story but I think she went directly to the media without a formal diagnosis so the media really scrutinized her. The journalists treaded her as if she was crazy because she claimed to have the odors though none of the journalists did. That woman appeared to have PATM imo, though she believed to have TMAU. I can’t find that video interview anymore. She had a PH.D. I think but was only a preschool teacher. If somebody finds the video, please paste it for everyone to see.

Ray sorry I didn’t read all your post, had things to attend, but I’ve just read 2 very interesting paragraphs.
@Ray, are you suggesting that we PATMers have a deficient FMO3 enzyme or another similar liver enzyme?
I’ve just scanned through the paper. Interesting but we’ll have to wait and see if they find the genes. There’s one thing I wish they’d reveal. Were these volunteers having it from what age. Birth? or later in life. That might shine more light in regards to our problem.

Also, if some of them had it later in life? Wouldn’t it be like Ellie James case where it was acquired? So unless the genes are identified and matched specifically to the dysfunctional FMO3 enzyme, there’d be still be a lot of questions about this.

Interesting findings, thanks for this.

@Ray2502, do you believe we have a dysfunctional FMO3 enzyme?
Hello dontgiveuphope,

I think we have more than 1 defective enzyme. This would explain why everybody that claims to have PATM, react differently to food. I have no issues with eating fish or beef and chicken but some other PATMER might think otherwise. Their PATM reactions might be triggered by the above mentioned foods but we can all agree that sugar and yeast products will affect us all.

I remember specifically more than  once, I was in the car with my family and my wife said that it smelled awful like rotten eggs and I could not detect it. She later told me that it was coming from me. My theory is that if we don't eat a PATM free diet, we could develop full blown TAMU2.

I have not had that happened to me again since I've been eating PATM free diet.
An update to the black seed experiment.

Black seed did not help with PATM reactions but it did reduce them.
Also, I bring this up again and again, sorry but vitamin D some how temporarily reduces PATM for me.
“I think we have more than 1 defective enzyme.”

I agree with you there. Imo if gut dysbiosis is proven to be wrong, I will only see the above hypothesis as the only explainable idea. Like you said it will explain the slight differences in what we observe. Given that the liver contain so many enzymes, it could be any of one or more involved.

I now believe that perhaps Ellie James who was formally diagnosed with TMAU2, probably had multiple failing liver enzymes. FMO3 enzyme and probably a few others which included one for PATM as well.

For me, personally regardless when, how and what I eat, I only make others allergic, which doesn’t have any odor at all. If my diet is very bad, others would just cough, sneeze and get sick much more quickly but there’s never been any accompanying odor. I was surprised to find others with odors in this forum. Perhaps it proves the diversity of this condition.

I’m on Vitamin D already. I had three bottles sitting in the fridge from last year I think. I haven’t checked the expiry date yet…lol. I’ll see if black seed helps.

Again, thanks for sharing your views.
I haven't seen any changes from Vitamin D but perhaps it's because I'm eating normally now. Besides I don't take as much as you do.
Hey @Ray2502, you know I was just thinking about vitamin D. We know from MeBO research that leaky gut is at the center of the problem of all digestion problems, including PATM. The formal definition is gut permeability. We know that Vitamin D affects gut permeability itself by allowing the rapid absorption of certain elements.

So I’m just thinking that perhaps that in the same process of causing the rapid absorption of Ca,K,Z, and PO ,it’s actually slowing or inhibiting the absorption of toxins or compounds associated with PATM, across the gut lining. In cellular biology there are many channels that actually work in opposite direction on cells. Cystic Fibrosis is actually caused by a problem on these channels caused a faulty protein. My speculation is, perhaps the large amount of Vitamin D you took somehow interfered greatly with the permeability of the gut. Just a thought.
Hey, did you do Gas chromatography–mass spectrometry (GC-MS) before?
Avatar universal
This is very promising because it has medical community behind it.  I myself feel PATM is very similar to TMAU like most of us do but we describe it as odorless TMAU.  

However I was at a site one time and the person said there is a smell in here,  I can't smell it when i'm in here but if I leave and come back I can.
Yes, it’s very hard to know for sure, but here’s the thing. PATM is uniquely classified by the fact doctors and family members can’t smell anything, because if they had, PATM would have been discovered long ago just like TMAU.

However, we know, regardless of whether it’s TMAU, PATM or anything else that we have, it is gut bacteria that produces the compounds, because what we eat, probiotics, and antibiotics determines how severe it is. In that case, I would guess, although rare, that occasionally some of us may develop some odor, because it just depends on the variation and ratio bacterial strains.

For instance, the case of Ellie James and 2 others that I have seen interviews of, they’ve been diagnosed with TMAU2 but have PATM symptoms as well. This tells me there are TMA production bacteria but there also PATM etc. producing bacteria too and perhaps other unknown strains, so what’s stopping some of us from having PATM and a little bit of TMAU odor too.

I myself have never had odor, but I believe perhaps 5% of PATMers might occasionally develop some odor at times.
Have you been tested for TMAU?
@dontgiveuphope negative
Thanks! That’s good news! I haven't been tested. It’s because I never had an odor to become suspicious it’s TMAU. Despite not having odor, over the years I noticed the similarities in almost everything else. For instance, the diet was similar – vegetarian seems to lower the severity of both conditions. Antibiotic (natural or artificial) seems to have an effect, negative or positive on both conditions.

TMAU2 patients have additional symptoms, beside the odor, that we have associated only with PATM i.e. coughing, sneezing, sniffling, flu-sickness symptoms.

And now MeBO has verified characteristics that are common to both and they still haven’t found something to differentiate the two. Again, I assume they will find it eventually, but it’s amazing how things are similar so far.

So far, PATM is not TMAU2 but very very similar in many ways…lol. What on earth could that mean? I just hope it’s not an enzyme problem, although it’s almost leaning in that direction now.

Ray2502 argued once that he’s done everything in his lifetime to tackle this problem and still wouldn’t get rid of it, he can only treat it…lower it but can’t cure it. I think if I remember correctly, ray2502 argued this is got to be a liver enzyme problem. Perhaps he’s right. We will get to know if it’s true as more results come from MeBO.


If it's a liver enzyme, then that'll be quite depressing. How do you explain people who develop PATM later into life such as after long courses of antibiotics. That would rule out any genetic enzyme deficiency, right?
Yes @smellyorus, I know it sounds depressing when we talk about that, I totally agree. But we are talking about TMAU2 here, not TMAU1. TMAU1 is the only genetic type.

TMAU2 is not known for sure how it starts. Some specialists think it’s gut dysbiosis, some think it’s enzyme deficiency. There’s never been a consensus. Both are possible. There have been cases where TMAU2 patients were cured by antibiotics so proves that those cases in particular were just gut dysbiosis.

But remember antibiotics and other drugs can easily change gut microbiota as they can ruin organs or enzymes permanently too.

So for PATM, yes, most of us were on antibiotics cycles before this happened. But it could mean both ways. Either our gut microbiota is having problems recovering to normal or liver enzymes have been screwed permanently. Clearly there’s no evidence to eliminate either one just yet.

Personally, I’m starting to lean towards the idea that probably there’s a liver enzyme problem. It is also possible our gut epithelial cell linings have some kind of faulty protein that makes the gut lining defective in some way.

Don’t think too hard about it. The evidence will come slowly.
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I’ve just read paper where a person had both TMAU1 and TMAU2…lol. Believe it or not, it is possible. What scientists found is that she had mutations on her FMO3 gene which flags her as having a partly functional liver enzyme (TMAU1) but the TMA urine test also show she had elevated TMA but normal TMA/TMAO ratio (TMAU2). They gave her antibiotics to lower the gut microbial overgrowth and TMA production went down but came back up again after a while…lol. Nature can be tricky.
So we’ve seen PATM, TMAU2, TMAU1, PATM+TMAU2…. and now TMAU1+TMAU2.
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