TMAU

[halitosisux]

Fascinating and insightful. It becomes more and more feasible the more these fundamental concepts are understood.

Conclusive evidence then of the incorrectness of the assumption that TMAU is only about mouth and body smelling like a dead fish and having BO like a tuna.

Conclusive evidence of the MAJOR role that saliva (and probably just about every other bodily secretion including the mucus) plays in infesting the mouth with odourous TMA, and that at low concentrations causes odours that resemble rotting trash, not fish.

Conclusive evidence that every single human being is teetering on the edge of having enough TMA in their bloodstream to cause noticable, if only transient amounts of foul breath, depending on how efficiently they can convert TMA, the dietary intake of TMA precursors, and the general condition and functioning of the digestive system. (sounds like quite a few people on here)

With what is known today, any long-term chronic BB sufferer who tends to have had their lives ruined and going round in circles having spent $$$$s and yet hasnt been tested for TMAU or AT LEAST tried some of the measures that are known to help diagnosed TMAU sufferers, just to see to see the effect on themselves, needs to have their head tested.

[caramiamine98]

Information on testing for tmau (primary and secondary):

Scientist42 wrote:

I would like to reiterate that Trimethylaminuria is a rare cause of breath/ body odor but secondary tmau (due to microbial overgrowth in the gut) is very much treatable! Hence, in my opinion anyone who suffers chronic breath/ body odour should exclude this possibility after seeing the doctor/ dentist first.

In particular, I would advise trying a low-choline diet and taking lactulose and probiotics long-term. This will give you some indication whether or not you are likely to have secondary tmau. Trying to get a physician to prescribe metronidazole may prove tricky unless you have tested positive for tmau.

Unlike in the U.S, here in the UK, secondary tmau is commonly tested (as well as primary tmau) by the various testing centres and my personal opinion is that there are now very good grounds for this, especially as this is one of the few causes of breath/ body odor which is treatable!

I have found that there are many people who tested negative for secondary tmau yet still benefit from lactulose/ probiotics and the occasional course of metronidazole. This suggests that microbial overgrowth in the gut may be the cause of some people's breath/ body odor.

viewtopic.php?t=2345

Scientist42 also wrote:

To my knowledge, the various TMAU testing centres in America don't specifically differentiate between primary and secondary tmau. Anyway, the important thing is that they measure the ratio of your TMA: TMAO which gives an indication of the conversion of TMA to TMAO.

Usually in America, patients having the test receive a choline load which they take orally and this high amount of choline guarantees that the FM03 enzyme will be challenged. So, a little while after taking the choline load a urine sample is taken and the levels of TMA and TMA Oxide in that sample are measured.
If most of the TMA remains unchanged (unoxidised) then that indicated you have primary TMAU.

A blood test is performed to look for mutations of the FM03 gene to confirm a diagnosis of primary tmau.

In the UK, patients are usually not given a choline load but are often told to take adequate choline in their diet in the run up to the test. People with primary tmau usually have very little of the TMA converted to TMAO. People with secondary tmau often have intermediate amounts of TMA converted to TMAO. People who don't have tmau will have excellent conversion.

In America, you basically have the same the same test but it is more specifically geared to testing you for primary tmau because you get a choline load. If you get an intermediate conversion but the blood test comes back negative then I suspect you will have secondary tmau however I think in America they will say your result is in the upper end of normal.

A lot of patients with primary tmau appear to have secondary tmau as well for some strange reason. This can be seen by the fact that metronidazole (antibiotic) treatment followed by use of probiotics etc succesfully reduce the odour in these patients. So, I think there is a lot of grey area.

My advice is to get both tests (urine and blood) done in America. If your blood result comes back positive then you have primary tmau. If it comes back negative but your TMA conversion was on the upper side of normal then you may have secondary tmau, and this is treatable using the TMAU treatment protocol. If your blood and urine test both come back negative then you may have something else or had a false negative.

The following websites are excellent-lots of articles, advice, etc

http://www.bloodbornebodyodorandhalitosis.com/

http://health.groups.yahoo.com/group/Trimethylaminuria/

http://www.bodyodorsupport.com/index.php

I guess that settles it, H. I'm moving to the UK! Hmm, I wonder who I could stay with while I'm getting tested? Somebody who would be sympathetic to my plight. I wonder who that could be...

[halitosisux]

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[caramiamine98]

Since I'm moving to the UK now, I've decided I want to live in an 'agricultural zone with it's normal ambient odour which everyone is used to and never really speaks about'. If I get tested here I have to do a choline load (otherwise known as MY WORST NIGHTMARE). If I get tested there I won't have to do one and I might better blend in with the other 'ambient odours'. Also, my doctor here is really mean. He yells at me, swears at me, calls me names, oh wait! That was you! How could I have forgotten?

All kidding aside, I have to thank Scientist42, Arun Nagrath for providing me with that last quote on my previous post. He was gracious enough answer my questions even though he was and is very busy. Thanks again.

Thank you for the hotel info, H. Are those the cheapest rates? Yikes! I'll have to start my tmau testing fund sooner than I thought...

[halitosisux]

lol, most places here in the UK are agricultural zones, particularly the town centres on a friday night.

GET YOUR $£%(£%$( TMAU TEST %*($£%*£( BLOODY ^*(£"WHAT ARE YOU WAITING FOR %*"(£

And kidding aside.. yes Arun is a thoroughly nice bloke who has done so much to help this cause - I wish I had the confidence to attend his meetings but im just so lost and anxious in social situations it would be a waste of time because i'd be completely consumed by this side of things. I'd end up ordering water instead of alcohol and everyone would just get distracted by my social ineptitudes

[caramiamine98]

Oh well, alcohol is bad for you anyway. I'd love to attend one of those Meetups. I think they would be a lot of fun. I don't know anyone like me so I think it would be great to actually get to meet people with the same or similar issues. I'll start saving my pennies now...

[halitosisux]

True.. and until I found this site nearly a year ago now, I had "compartmentized" my BB (if u know what I mean), in other words I'd just moulded my life so well around my problem that I could live with it. Infact, as far as people were mostly concerned I was even GAY, but I was just so numb it was so irrelevant like most things in my life had become. So you can imagine the mess I'm dealing with inside as a person on every level.

So, for years I wasnt actively dealing with my BB anymore, and had hardly used the internet in what I'd done so far up to this point. Spent $$$s on books and travelling to different cities to read in their libraries, so I could focus without stumbling across anyone I know finding me reading about tongues etc like I needed to become any more bizarre than I already was.

So yes, until I found this site I never knew anyone else like me either. I SWEAR that until I found this site last year, I felt like the only person on the planet who suffers so physically and psychologically because of bad breath - I have still NEVER seen anyone take any of the measures I'd take to hide from it, I was supersensitive to anyone being able to smell me. Holding my breath and grunting my words out etc. Running for dear life at the prospect of having to sit with others in the middle of a back seat of a car - i'd rather be buried alive. Sometimes pretending to go NUTS if I felt a trapped situation was looming. I could go on and on. So its been FANTASTIC to share and read of others in the same boat. I really cant imagine a more humbling human experience than enduring the only life you've ever known with this problem, amongst free people.

And that's just meeting people on here, so to meet others in real life would be the most therapeutic ever thing I think.

[caramiamine98]

For anyone who is on a low choline diet:

Lymphocyte gene expression in subjects fed a low-choline diet differs between those who develop organ dysfunction and those who do not2

Mihai D Niculescu, Kerry-Ann da Costa, Leslie M Fischer, and Steven H Zeisel
Department of Nutrition, School of Public Health and School of Medicine (MDN, K-AdC, LMF, and SHZ), and the Nutrition Research Institute (SHZ), University of North Carolina at Chapel Hill, Chapel Hill, NC.
Reprints not available. Address correspondence to SH Zeisel, Nutrition Research Institute, School of Public Health and School of Medicine, University of North Carolina at Chapel Hill, CB# 7461, Chapel Hill, NC 27599−7461. E-mail: [email protected].

Abstract

Some humans fed a low-choline diet develop hepatosteatosis, liver and muscle damage, and lymphocyte apoptosis. The risk of developing such organ dysfunction is increased by the presence of single-nucleotide polymorphisms (SNPs) in genes involved in folate and choline metabolism.

Objective

We investigated whether these changes that occur in the expression of many genes when humans are fed a low-choline diet differ between subjects who develop organ dysfunction and those who do not. We also investigated whether expression changes were dependent on the presence of the SNPs of interest.

Design

Thirty-three subjects aged 20−67 y were fed for 10 d a baseline diet containing the recommended adequate intake of choline. They then were fed a low-choline diet for up to 42 d or until they developed organ dysfunction. Blood was collected at the end of each phase, and peripheral lymphocytes were isolated and used for genotyping and for gene expression profiling with the use of microarray hybridization.

Results

Feeding a low-choline diet changed the expression of 259 genes, and the profiles of subjects who developed and those who did not develop signs of organ dysfunction differed. Group clustering and gene ontology analyses found that the diet-induced changes in gene expression profiles were significantly influenced by the SNPs of interest and that the gene expression phenotype of the variant gene carriers differed significantly even with the baseline diet.

Conclusion

These findings support our hypothesis that a person's susceptibility to organ dysfunction when fed a low-choline diet is modulated by specific SNPs in genes involved in folate and choline metabolism.

To read the rest of the article see:
http://www.pubmedcentral.nih.gov/articl ... d=17616785

[caramiamine98]

Info from the National Institutes of Health Genetic and Rare Diseases Information Center (GARD)

How might trimethylaminuria be treated? 

Although there is no cure for trimethylaminuria, it is possible for people with this condition to live normal, healthy lives. The following are some ways a person with trimethylaminuria can reduce symptoms of odor:

-Avoiding foods containing trimethylamine and its precursors (choline and trimethylamine-oxide). Trimethylamine is present in high levels in milk obtained from wheat-fed cows. Choline is present in high amounts in: eggs; liver; kidney; peas; beans; peanuts; soy products; brassicas (brussel sprouts, broccoli, cabbage, and cauliflower); and lecithin and lecithin-containing fish oil supplements.  Trimethylamine N-oxide is present in seafood (fish, cephalopods, crustaceans). Freshwater fish have lower levels of trimethylamine N-oxide.

-Taking low doses of antibiotics to reduce the amount of bacteria in the gut. This suppresses the production of trimethylamine.

-Taking laxatives can decrease intestinal transit time and reduce the amount of trimethylamine produced in the gut.

-Taking supplements to decrease the concentration of free trimethylamine in the urine.

-Activated charcoal taken at a dose of 750mg twice daily for ten days.

-Copper chlorophyllin taken at a dose of 60mg three times a day after meals for three weeks.

-Using soaps with a moderate pH, between 5.5 and 6.5. Trimethylamine is a strong base (pH 9.7) thus soaps with pH closer to that of normal skin help retain the secreted trimethylamine in a less volatile form that can be removed by washing.

-Taking riboflavin (vitamin B2) supplements to enhance any residual FMO3 enzyme activity. Recommended intake is 30-40mg taken 3-5 times per day with food.

-Avoiding factors that promote sweating, such as exercise, stress, and emotional upsets.

http://rarediseases.info.nih.gov/GARD/C ... nuria.aspx

[17yearbattle]

Why get tested for TMAU if there's no cure for it.. why get tested for TMAU if you dont have persistent BO or any abnormal BO at all? Why get tested for TMAU if the only treatment is diet management and antibiotics? Haven't we all tried these any way?

Im just saying...

Lets stay focused!

[halitosisux]

LOL why get tested for TMAU if there's no cure? Ummmm because you would then at least know what causes your BB and save yourself spending the rest of your life chasing something that doesnt exist.

This site is about sharing information so that people can try the obvious things that are generally associated with BB. But you also have to consider it might be due to the very rare causes, such as TMAU or something very closely relating to it, even things which are as yet to have been identified. TMAU was only ever investigated because of its curious smell of FISH, so it wasnt difficult to work backwards to isolate this. TMAU is due to a genetic flaw of a particular enzyme system. People who dont have this flaw dont get TMA building up in their bloodstream to the same levels. In low quantities TMA smells nothing like fish, but rotting garbage and other foul odours. And you dont have to have this genetic flaw to end up with high levels of TMA in your blood/saliva and other secretions, even just eating a pile of eggs will raise the level once its been digested. Your intestinal bacterial flora alone, if its been disturbed or overgrown with unfavourable species (whatever they might be), can give rise to increased levels of TMA production from the basic foods you eat. This is all related to something called secondary TMAU and you cant just rely on the presense or the absense of body odour to determine whether this is your cause or not, because there are no definite correlations.

Diet management and antibiotics can have a detrimental effect as well as a beneficial effect, depending on what it is you are targeting or trying to achieve. It hangs in the balance and the therapy is strict, so the balance can swing depending on what you do with these weapons.

@Cara, the B2 effect on enhancing FMO3 enzyme activity is interesting, considering that so many people have reported how B2 helps with their BB. Not saying it relates directly with TMAU but that it might involve other similar enzyme activity connected with BB.

[caramiamine98]

New TMAU document from Nigel Manning, Principal Clinical Scientist of Dept. Clinical Chemistry at Sheffield Children's Hospital in England which is the only known TMAU genotype test lab in the UK.

TMAU – diagnostic testing at Sheffield Children’s Hospital


Nigel Manning Dept. Clinical Chemistry, Sheffield Children’s Hospital,
Sheffield UK.

Introduction

The phenomenon of ‘fish odour’ has been reported for many centuries. More
recently attributed to the tertiary amine trimethylamine (TMA), the ammoniacal
body odour like the smell of rotting fish can have severely detrimental effects
on the lives of those suffering from ‘Fish Odour Syndrome’. Now more
commonly referred to as Trimethylaminuria or TMAU, patients with this
unfortunate condition exhibit increased excretion of TMA in urine as well as in
sweat and breath vapour. The main causes of TMAU, low hepatic TMA
oxidation and intestinal overproduction of TMA give rise to the two main types
of the disorder.

The inherited form of TMAU is known as Primary TMAU (TMAU1). The result
of a faulty autosomal recessive gene, TMAU1 patients have impaired activity
of a liver enzyme flavin-containing mono-oxygenase type 3 (FMO3) which
oxidises a wide range of substrates including many drugs. TMA is oxidised to
non-odorous TMA-oxide (TMO) by FMO3 which can then be excreted. TMA
itself is generated in the large intestine by bacterial degradation of compounds
such as choline (high in liver, eggs and beans/peas), carnitine (meat) and
TMO from seafood (TMA from fish ‘spoilage’ has been attributed to several
species of Vitrio and Shewanella bacteria).

TMAU1 therefore results from FMO3 deficiency with an increase in the ratio of
TMA to TMO in urine which can be used for diagnosis.

Due to the broad spectrum of substrates oxidised by FMO3, TMAU1 patients
may suffer from adverse reactions with many drugs including codeine,
tamoxifen, ketoconazole, nicotine, cimetidine, ranitidine and phenothiazine.
Hypertension may result from ingestion of red wine and cheese (and
chocolate), which produce the neurotransmitter tyramine, another FMO3
dependent compound. Many people suffer from migraines associated with
tyramine containing foods and perhaps FMO3 deficiency may explain some of
these cases, but overall this demonstrates the adverse medical
consequences of TMAU1 as well as the odour related psychosocial aspects.
The acquired form of TMAU is covered by the term Secondary TMAU
(TMAU2) where TMA excretion is high even though FMO3 activity is normal.
Most TMAU2 patients produce too much intestinal TMA due to excessive
bacterial growth of TMA-generating species. The TMA burden is so great that
FMO3 oxidation produces large amounts of TMO but (in most cases – but not
all) is still unable to oxidise enough TMA to prevent an excess. This problem
may be exacerbated by intestinal structural problems such as ‘blind loops’ or
post- operative complications. TMAU2 usually presents in adulthood although
children have been known to acquire excessive TMA-producing bacteria with
the resultant odour.

The diagnosis of TMAU2 depends on the detection of increased urinary TMA
and TMO with a normal TMA/TMO ratio indicating normal oxidation by FMO3.
Patients with liver or kidney disease have been known to produce a TMAU1-
like pattern of excretion, although due to a secondary cause. Importantly this
may also occur with a urinary tract infection (UTI) which results in TMA being
produced directly into the urine giving a false positive result. Whenever results
suggest TMAU1, therefore, UTI must always be excluded by microbial
analysis before a TMAU1 diagnosis can be confirmed in a follow-up sample.

Testing for TMAU

The urine test consists of two measurements:
a. trimethylamine or ‘Free’ TMA
b. TMA-oxide [+ free TMA] = ‘Total’ TMA.

The technique currently used in our laboratory is gas chromatography – mass
spectrometry (GCMS) analysis of the ‘headspace’ vapour of heated,
alkalinised urine. This method superseded a direct injection MS method used
from 1997 until 2002. Results from the two methods compared well, although
the current methodology allows for automated headspace sampling and
GCMS injection.

A positive result is usually followed up with a routine second test after a report
of the initial findings. The turnaround time for the test is currently 4 weeks or
less. A GP or physician referral is essential, but we can offer advice by phone
or email about how to start the process.

DNA analysis for the FMO3 gene is also now available with a turnaround time
of 8 weeks. The genetic test provides the vital confirmation required for a firm
diagnosis of TMAU1 and has demonstrated that the TMA / TMA-oxide ratio
may normalise in TMAU1 due to spurious increases in urinary TMA-oxide.

Results and Diagnoses

We tested 1150 urines from 716 individuals from 1997 to 2009.
379 results indicated significant TMAU.

Many TMAU sufferers may restrict their diet before testing in an effort to
reduce odour. This may occasionally affect an initial diagnosis as TMA
excretion may be sufficiently reduced to normal or give a normal Free to Total
TMA ratio (less than 21%). For diagnostic clarity it is essential that the sample
is collected when odour is at it’s maximum. This may necessitate creating the
conditions which induce the odour such as dietary intake of choline (eg
pulses, eggs, liver), carnitine (red meat) and trimethylamine oxide (seafood).
Dietary ‘loading’ is possibly most effective when restricted to a simple high
choline meal of 2 eggs and 400g baked beans. Previously choline
monohydrate was an effective loading agent but has become difficult to obtain
as a chemical for patient administration. The effect of choline loading and
diagnostic clarification achieved by loading can be seen in the following case
report.

A case of choline load to aid diagnosis in a case of TMAU:

An adult presenting with a significant odour was tested for urinary TMA. The
results showed both an increased TMA and Free/Total TMA ratio, which
indicated a possible primary defect (TMAU1). [Fig.2]

A repeat 24 hour acidified sample however gave a normal Free/Total ratio,
with increases in both the Free and Total TMA – suggesting the possibility of
increased oxidation in response to an increased Free TMA burden (a possible
indication of TMAU2).

Antibiotic therapy was commenced and resulted in the normalisation of Free
TMA although the Total TMA was still increased (again an indication of
increased oxidation in response to increased intestinal output of Free TMA).
For clarification a 5 gram choline monohydrate load was given to the patient
and samples collected for 72 hours after load.

Total TMA showed a dramatic increase (with Free TMA) and the Free/Total
ratio remained within normal limits. Gradually the Free and Total TMA
reduced to nearly normal excretion values.

These results indicated a treatable TMAU2 . The first result was probably due
to a urinary tract infection or bacterial contamination of the inital sample which
had not been acidified). The patient was further treated with antibiotics to
eradicate enterobacterial overgrowth.

Discussion

GCMS analysis of headspace vapour of alkalinised urine with stable isotope
dilution provides a robust method to measure both free and total TMA for the
diagnosis of TMAU1and 2. Differential diagnosis can be hampered by genitourinary
infections and intermittent presentations which may reflect TMAU1
carrier status.

Treatment of both TMAU1 and TMAU2 is based on diet to restrict the sources
(precursors) of TMA and antibiotics to eliminate the TMA-producing bacteria.
TMAU2 can in fact be cured by eradication of the excess bacteria, although
stubborn colonies may re-grow to excess and require further courses of
treatment.

TMAU1, as a genetic defect, cannot be completely cured although therapy
(dietary and antibiotic) can successfully control the patient’s free TMA to a
less odorous level. Patient’s residual enzyme activity is variable depending on
the specific mutation and as such trials with the cofactor riboflavin have been
tried with some success. Milder TMAU1 patients can, however, reduce their
TMA to almost normal values with just diet and periodic antibiotic therapy.
Other forms of therapy are based on the neutralisation of TMA chemically.
Skin creams with a comparatively low pH (5.0) may neutralise alkaline TMA.
This creates a non-volatile salt of TMA which lessens any odour and can be
washed off by the patient later. Another solution lies in deodorising tablets
such as ‘activated charcoal’ or copper-chlorophyllin complex (marketed as
‘Nullo’). These ‘internal deodorants’ have been successfully used for many
years and would be ideal for more severely affected TMAU1 patients.
Detection and perception of odours varies between individuals. Some people
are odorous to friends, family and work colleagues but are unaware of an
odour, whilst others maintain they are odorous but those around them would
not agree. For those individuals who are sufficiently motivated to seek medical
help, the type of odour is often difficult to describe, but ranges from ‘chemical’
to ‘faecal’. ‘Rotten fish’ or ‘ammonia-like’ is not always mentioned, but TMAU
seems to have become a focus for all malodours, possibly due to awareness
of the disorder, the availability of a test and the possibility of a diagnosis.
A significant cohort of sulphurous or faecal odours have been reported by
individuals who contact the laboratory. This may be another enterobacterial
problem, but although Shewanella species are known to produce both
hydrogen sulphide and TMA, we have yet to measure an increased TMA or
TMO as a secondary marker for enterobacterial overgrowth in these cases.
For those with a significant TMAU, difficulties in diagnosis mainly stem from
the interpretation of TMA and free/total ratios given the background of diet,
variation of enzyme activity and variation of bacterial sources of TMA. This
can be summarised by the sub-types of presentation and biochemical
abnormality we have encountered over the past 12 years. The new FMO3
mutation service should help to clarify TMA results greatly in the years to
come.

TMAU1 and TMAU2 possible sub-types:

a. TMAU1 transient neonatal – possible delay in switch from fetal enzyme
FMO2 to FMO3 TMA oxidation, but resolves during development.
b. TMAU1 severe childhood - parenting / schooling problems are possible.
c. TMAU1 adulthood – probably presented in childhood; long-term sociopathy.
d. TMAU1 heterozygote – may present only during dietary load / menses.
e. TMAU1 very mild – ‘double dose’ DNA polymorphisms – TMA borderline.
f. TMAU1 FMO3 mutation proven TMAU1 with increased TMO (like TMAU2)

a. TMAU2 severe neonatal -‘sepsis’ massive TMA responds to antibiotics.
b. TMAU2 childhood - antibiotic eradication prevents school / social problems.
c. TMAU2 adulthood – may have long history of odour, eradication possible.
d. TMAU2 intermittent – difficult diagnosis without precursor load.
e. TMAU2 due to UTI – presents biochemically as TMAU1 (urine-only odour).
f. TMAU2 due to renal or hepatic dysfunction – presents as TMAU1.

References:
Ayesh R, Mitchell SC, Zhang A, Smith RL (1993) The fish odour syndrome:
biochemical, familial, and clinical aspects. Brit Med J 307: 655-657.
Chalmers RA, Bain MD, Iles RA (2003) Diagnosis of trimethylaminuria in children:
Marine fish versus choline load test. J Inher Metab Dis 26 (Suppl 2): (448-P) 224.
Fraser-Andrews EA, Manning NJ, Ashton GHS, Eldridge P, McGrath JA, Menagé H
(2003) Fish odour syndrome with features of both primary and secondary
trimethylaminuria. Clinical and Experimental Dermatology 28: 203-205
Humbert JR, Hammond KB, Hathaway WE, Marcoux JG, O’Brien D (1970)
Trimethylaminuria: The fish-odour syndrome. Lancet 2:770-771.
Lee WG, Yu JS, Turner BB, Murray KE (1976) Trimethylaminuria: Fishy odors in
children. New Eng J Med 295: 937-938.
Mitchell SC (1996) The fish odour syndrome. Perspectives in Biology and Medicine
39 (4)
Treacy EP, Ackerman BR, Chow LML et al (1998) Mutations of the flavin-containing
monooxygenase gene (FMO3) cause trimethylaminuria. A defect in detoxication.
Hum Mol Genet 7: 839-845.
Treacy E, Johnson D, Pitt JJ, Danks DM (1995) Trimethylaminuria, fish odour
syndrome: a new method of detection and response to treatment with metronidazole.
J Inher Metab Dis 18: 306-312.

http://www.bloodbornebodyodorandhalitos ... -from.html

or in PDF form (includes graphs)

http://www.meboresearch.com/2010%20ARTICLE%20TMAU.pdf

[halitosisux]

Good info there C.
If I still had BB I know I'd want to find out. Just imagine how many people will go through life having a TMAU related condition and never know about it.

[caramiamine98]

!7yearbattle,

While it’s true that primary TMAU (TMAU1) the genetic kind is not currently curable it can be managed by the aforementioned protocols although they don’t always work for everyone. Secondary TMAU (TMAU2) the acquired kind is treatable. There are people who have been diagnosed with secondary TMAU that only have BB and not BO.

H,

Yeah, it’s a great paper. The PDF version is easier to read plus has charts and graphs. I hope it clears up any confusion people have this subject. As for vitamin B2, I didn’t know that many people have found it helpful for BB. That’s interesting. Most of the B vitamins are helpful in that department it seems. Cheers C.

[wenjie]

Nice post vonreall, thank you for all nice thoughts. Look I am not going to get tested for tmau. I hate doctors somehow. I always felt strong sideeffects after taking drugs, antibiotiscs so I just do not visit them anymore. Also they do not give me a solution. I had checked all my main organs few years ago and I remember how my father got ****ing abusive after we came back from stomach checkup, and the doctors could not find nothing really wrong.

He went ballistic, like always when I dared to talk with him about bad breath.

I am wondering am I the only one who have such abusive parents and also have bad breath. I have not read about others having such major problems with parents.

Like I have the feeling that your parents still like you though you have bad breath.

I think I will never speak with my father again. He was a real prick just looking me thru the bad breath point of view. Once I rememer he entered my room when I was crying and he screamed stop crying - do you want me to pour water on your head.

And how can a parent call his child a pig .............

I am happy for you others that you do not have to have such abusive parents.

my parents have done the same thing to me like yours.My bb is really serious just like yours too.