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Tuesday, April 20, 2010

Menstruation and transient trimethylaminuria

Very few researchers have been interested in Trimethylaminuria, and very few papers published, especially over the last few years, since the genetic coding of FMO3 was discovered and then interest waned.

Probably 2 with the most interest would be Dr John Cashman in San Diego (HBRI) and The Laboratory of Drug Metabolism and Pharmacokinetics, Showa Pharmaceutical University, led by Professor Yamazaki. The Japanese professor keeps a website on TMAU and seems to keep an interest in the subject.

In 2007, the 2 Dr's colluded to follow 5 cases of females who had compromised FMO3 function to varying degrees, and test their urine over 120 days to follow the result pattern, particularly to see how menstruation affected FMO3 function. Interestingly, only 2 of the cases are regarded as being 'TMAU' positive. The other 3 are regarded as normal (not having 2 mutant copies of FMO3), and yet all of them had lowered FMO3 function during menstruation.

Case A would be regarded as a 'true' textbook TMAU case, 2 mutant copies, and over the 120 days her FMO3 function was indeed very low over the whole period (under 50%), especially during menstruation.

Case B was homozygous for 1 common 'polymorphism', which are regarded as far less serious 'mutants' than real mutant DNA copies. Her FMO3 function was generally around 90% except during menstruation when it could dip to almost 0%

Case C was heterozygous for 2 common polymorphisms, and her FMO3 function was normal except around menses when it could reduce to around 60% function.

Case D & Case E were homozygous for wild FMO3, and also had normal function, but with a decrease in function to around 60-80% function around menses.

The conclusion seems to be that any female harboring 2 copies of any type of FMO3 enzyme known to not be 'perfect', whether 2 mutant copies, 2 polymorphism copies, or 2 wild types, may be prone to decreased FMO3 function around menstruation. It would be interesting to see how a female with one mutant copy would get on, or to a lesser extent, a female with one copy of a polymorphism or a wild type, to see if they were also at risk.

Looking at the TMA levels alone (not the TMA-oxide levels), the numbers aren't given, but it looks as if case A was always above 10.5 mmol, which is generally around the level accepted where TMA smells may become an issue. Case A seems to always be above 10.5, whereas the other 4 only seem to be above 10 around menstruation. It would be interesting to know why the TMA levels rise in the case of B,C,D and E. It is as if FMO3 plays some role in containing the bacteria causing TMA.


Anonymous said...

Can you explain how the genes relate to the bacteria? I thought these were two different forms of TMAU. We know that killing the bacteria does not cure TMAU...last sentence is really misleading

Apr 21, 2010, 7:36:00 PM
bloodbornebodyodor said...

Hi. I wrote the article. With TMAU, there are 2 factors to consider : 1 is the amount of FMO3 you have. The other is the amount of TMA-producing bacteria in your gut you have. The point I was making was speculative, that I found it strange that when their TMAO level decreases, the TMA level seems to rise. Now that I think about it, maybe the amount of TMA was always the same but now not so much of it was being converted to TMAO, which would explain the rise. Originally, I couldn't see why the TMA level should automatically have to rise when TMAO goes down, as if the bacteria is becoming more abundant ,which I can now see may be a wrong assumption. In theory, if all the ladies could get their TMA levels down to normal levels, I would have thought they should not be expected to smell even if they have genetic TMAU

Apr 21, 2010, 8:29:00 PM
Anonymous said...

Thanks for the clarification. I did not find anything about bacteria in the study, it seemed that the genetic mutation was probably effected by hormones. Being a TMAU sufferer I would hate to have lay-persons telling me to take some antibiotics to get rid of the bacteria and be cured! :)

Apr 26, 2010, 4:06:00 PM
bloodbornebodyodor said...

In the end, it is TMA that causes the smell, so if you can get that below the 'smell-threshold' (around 11 micromoles ?) ... if TMA is causing the smell then in theory one shouldn't smell. The problem is, if someone has genetic TMAU, they cannot convert TMA to non-smelly tmao so well, and so have a far lower threshold. A normal person could tolerate 100micromoles of TMA absorption and convert probably 95% of it, leaving 5micromoles of smelly TMA. Someone with genetic TMAU, say they have 50% FMO3 capacity, if they took 100 micromoles they would be left with 50micromoles of smelly TMA. So someone with genetic TMAU has a much lower TMA threshold.

With the low choline diet, the aim is to starve the bacteria of it's food (choline). With antibiotics, it's to kill it. But we don't know the longterm problems with frequent antibiotic use, so I presume they suggest low-choline as the main approach.

If you look at case A, she was always above 11 and seemed to not be able to convert very much of the TMA to TMAO. It would be interesting to know if she was attempting to control the TMA level in the study. It would be interesting to know how much daily TMA a normal person typically absorbs and how difficult it would be to get someone with 0% function to be under 11micromoles. I presume very difficult. In the youtube video with the lady, she got her TMA level down from 45 to 15, but I don't know her full TMAU situation.

Once MeBO becomes a charity we hope to do small studies looking at these sort of scenarios. Hopefully we can apply for small grants and investigate.

Apr 26, 2010, 11:10:00 PM
Anonymous said...

You said: "With the low choline diet, the aim is to starve the bacteria of it's food (choline). With antibiotics, it's to kill it." Can you point me to where you found this information?

Apr 27, 2010, 1:55:00 PM
bloodbornebodyodor said...

It's my understanding that choline is avoided because it is altered by bacteria in the gut, one of the bi-products being trimethylamine. Maybe 'starve' is the wrong word, but we avoid choline so bacteria can't alter it. The problem if someone is genetic is that they have a much lower tma tolerance level, whereas someone with TMAU2 is generally regarded as having a 'gut infection', and so shold be ok if they get the bacteria down to 'normal' levels ?

Nigel Manning said :
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.

Presumably he is pessimistic about TMAU1 cases getting below the tma threshold but I presume everyone wants to aim for that.

Other expert quotes:

"Trimethylamine (TMA) is a tertiary amine derived from the enterobacterial metabolism of precursors such as choline and phosphatidylcholine present in the diet"

itself is generated in the large intestine by bacterial degradation of compounds
such as choline (high in liver, eggs and beans/peas), carnitine (meat)

Attempts to reduce the intake of precursors of trimethylamine such as carnitine and choline, through dietary management, appear to have been successful in some patients but not in all. It appears likely that dietary management might be most effective in mild to moderate forms of fish odor syndrome arising from particular mutations or haplotypes (Danks et al., 1976;Mitchell, 1996). Occasionally, a short course of neomycin and metronidazole to reduce the activity of the gut microflora and suppress the generation of trimethylamine have been said to be effective in some, but once again, not all cases

Apr 27, 2010, 4:51:00 PM
Anonymous said...

Thank you, That is what I did not understand!

Apr 27, 2010, 10:36:00 PM
bloodbornebodyodor said...

You are welcome. I did get a bit overly confusing. Also, my original sentence we started discussing from the post is probably wrong (once I worked out the arithmetic), which didn't help.

Apr 28, 2010, 9:01:00 AM
Wendy said...

I'm new here, so not sure how to do this. I was reading on TMAU during menses. It all seems to be connected to hormones. When certain hormones levels are raised, such as maybe estrogen, it seems to get worse. Could a possible treatment be a hormone that suppresses estrogen, or whatever the "problem" hormone is. If TMA rises during menses, I'm not a doctor, but I think when estrogen rises, then goes back down after menses, wouldn't lowering estrogen levels keep the tma down. Just a theory??? I have gotten comments lately of a fecal odor and have also been told I have estrogen dominance. Have also done the urine test at Arkansas Childrens's hospital and came back with a 6.817. The test said 6.8 was normal. And my test read: "mild TMAU." I keep seeing 10 or 11 as normal? Is that just different for US than London? I'm sorry if I did not leave this in the proper "space," but as I said, I'm new! Thank you. Wendy

Apr 30, 2010, 1:03:00 PM
bloodbornebodyodor said...

Hi Wendy.

That is interesting about Arkansas. I refer to around '11 umol/mmol' because this is the 'borderline' in the UK testing. So few labs test for TMAU that they probably all set their own reference ranges. Arkansas does not test for TMA-oxide, which means they can't work out your FMO3 efficiency. I guess they figure, if someone has a high TMA level, they will smell.

There's so little research into TMAU that all we can do is assume the FMO3 enzyme becomes temporarily inhibited during menses in some women. It will be to do with hormones, but not sure if we can assume it is estrogen yet. In the end, hormones are chemicals and perhaps can have some effect on body enzymes. It is also known that indoles in some foods (like cruciferous vegetables) can also inhibit FMO3. It woudln't surprise me if estrogen is detoxified largely/completely via the FMO3 enzyme. Anthing that worked for these ladies would only have an effect on those who solely have a smell problem during menses.

More research needs to be done.

Apr 30, 2010, 5:02:00 PM
mpdela said...

Hi Wendy,

Hi Wendy, I'm out of town now and don't have all the info here with me but I do know of a few women who have done hormonal therapy with birth control pills. Of course you would need to consult with your gynecologist before attempting any hormone treatment.

Apr 30, 2010, 10:01:00 PM
Anonymous said...

I hope this message works I have tried already.

I just wanted to ask if this website would be interested in providing some info on Biofilm. Biofilm is a slimy bacteria with a stick surface and other bacteria and fungus adhere to it. A protective coating is formed (film) and the various bacteria and fungi form a community.

The scientific field are very interested in biofilms at the moment and believe they cause inflammatory disease such as CFS, FM etc. They can also cause body odour, so could be interesting.
Also the Marshal Protocol is an unconventional new way of trying to treat patients with inflammatory disease without meds. These patients are suffering from BO while on the programme - could be a die off, but vey interesting.

Just a suggestion.

May 18, 2010, 6:52:00 PM
Anonymous said...

How can you test your FM03 function? I only have issues with smell when I have my period. I would like to know what type I have. and wouldn't it be great to be able to test at home so you would know if you were having a lower functioning day (I can't smell my own smell so I never know when it's happening = 100% paranoid all the time). This is a facinating article - thank you!

May 28, 2012, 3:18:00 PM
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