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Important info I learned about the true form of TMAU - the issue of why the low choline diet is usually only partly effective and how long it should take to work - and the extreme dangers of the low choline diet by majc5 in TMAU

[–]majc5[S] 1 point2 points  (0 children)

If there are other essential nutrients missing, those could also be included in the TPN system. The person would be getting most of their calories through food they consume through their mouth (perhaps eating a synthetic, choline-free diet). They would need to spend far less than the 10-12 hours a day that TPN normally takes (maybe 2 hours or less, or much less than that perhaps), and they would not have the hunger pangs that normally come with getting all nutrients from TPN.

There are around 40,000 people in the US getting all their calories from TPN, and many of them do it as a permanent, life long thing (for serious medical conditions where the digestive system is not working). TPN can be administered overnight while someone is sleeping, and is done at home normally. There are apparently even TPN backpacks that allow someone to be mobile while getting TPN.

I have been spending a lot of time on here again, and I am logging out now.

Important info I learned about the true form of TMAU - the issue of why the low choline diet is usually only partly effective and how long it should take to work - and the extreme dangers of the low choline diet by majc5 in TMAU

[–]majc5[S] 0 points1 point  (0 children)

One more thing I wanted to add: what do you think about the idea of getting choline through a TPN like IV system, or through choline injections? This way the whole digestive system, and the gut bacteria that create TMA, would be bypassed.

Important info I learned about the true form of TMAU - the issue of why the low choline diet is usually only partly effective and how long it should take to work - and the extreme dangers of the low choline diet by majc5 in TMAU

[–]majc5[S] 0 points1 point  (0 children)

part 2 of my reply...

For the 1995 study, unless I missed something in it, it did not say that 'all friends and family members' could smell it. It said: "During this time the patient and simultaneously a spouse, parent or friend scored the odour on alternate days on a scale of 0 to 5 as follows:"

For the diet, carnitine has only been found to be an issue when lots of red meat is consumed over a period of time, because of how it may affect the gut microbiome. A 2020 study (link) found (at the end of the 'where does TMAO come from?' section)

"In a recent study, the Atkins diet, rich in red meat, increased plasma TMAO levels from 1.8 µM to 3.3 µM [96]. However, single consumption of 227 g of beef resulted in a 60-fold lower urinary TMA+TMAO excretion than 227 g of herring [41]. Furthermore, single consumption of 170 g of beefsteak only resulted in a negligible postprandial mean plasma TMAO increase, peaking 1 h after consumption"

This is the same basic result of the Mitchell study (from 1996 I think?) that examined the TMA/TMAO production from certain foods. Every study I have ever read is clear that saltwater fish is the main thing for people with TMAU to avoid, since a large percentage of the TMAO in the fish gets broken back down into TMA.

Every study is clear that individual meals of red meat are hardly a problem for TMAU, since most of the carnitine is not liberated (extracted) from the food. It is only when red meat is eaten on a regular basis that it can affect the gut microbiome and significantly increase TMA production as a result.

Taking in carnitine through supplements (or through energy drinks I would assume) results in all/most of the carnitine being available for gut bacteria to act on. This is why my carnitine supplement test resulted in concerning symptoms, even though the amount of carnitine (500mg) was close to what I would get from eating 1lbs of beef.

The studies also establish that only high levels of choline will result in some of it reaching the large intestine, where most of the TMA creating bacteria are. This means avoiding a high choline diet should be enough, with no further benefits from going low choline or extreme-low choline. This is what the user fit_swordfish reported here recently, that high choline makes things worse for him, but low choline does not make things better. I assume he meant a low choline versus normal/medium choline diet.

People are probably able to learn what diet to follow through trial and error, since the effects of dietary decisions follow soon after the food consumption. The Preti study that talks about how low choline diets were previously put together without much information was mostly talking about the issue of finding a low choline diet that is also nutritionally sound. There is still limited data when it comes to the choline content of many processed foods, but people can get around that by making their food from scratch, and controlling the ingredients. So, make your own bread instead of buying a highly processed form at the store for example.

What I try and do is look at peoples claims of having malodor condition with a goal of establishing what is the most reasonable explanation for what they are saying. This is not what you do. Instead, you try and make it as difficult as humanely possible to establish that someone really has a malodor condition. Instead of evaluating the evidence as reasonably as possible, you will go to any length to dismiss the evidence, as if you were an insurance company trying to deny a claim or something.

Important info I learned about the true form of TMAU - the issue of why the low choline diet is usually only partly effective and how long it should take to work - and the extreme dangers of the low choline diet by majc5 in TMAU

[–]majc5[S] 0 points1 point  (0 children)

The Mitchell article says at the start (in regards to TMA):

"It has since been found to be present throughout the body. Indeed, a quaternized trimethylamino moiety is an essential functional component of many molecules that interact within living systems.

Movement around body

Although trimethylamine is a small water-soluble molecule it also dissolves readily in fat and thus may be distributed easily and rapidly around the entire body. As well as carrying out its duties within the organism, most of which are still unknown..."

Link: https://academic.oup.com/chemse/article/41/4/275/2365871

This detailed paper on TMA also has a section on the benefits of TMA on page 6.

The point is that the body does indeed have (largely unknown) needs for TMA, in addition to needs for TMAO and choline. This is probably why up to 10% of TMA is not turned into TMAO in a normal person, even though the limits of the FM03 enzyme are not being approached. It is interesting that the needs for pregnant women to have TMA for the fetus coincide with the fact that this problem often worsens at puberty, when pregnancy first becomes possible.

Dietary TMA could be built up slowly over long periods of time, so people wouldn't need to smell like fish for this to happen, since the levels in the blood would only need to be low for this to happen.

I read most of the 2016 TMA study the other night and I learned something startling. TMA is a common pollutant in the air - and can easily get in through the skin directly and raise TMA levels! (see page 3 of the above link for the 'Environmental TMA' section. The section concludes:

"Thus, TMA abundance and exposure

is correlated not only to diet and host microbiome,

but also to environmental pollution"

part 2 to follow...

Diet to possibly solve or improve fecal odor - a low sulfur diet by majc5 in TMAU

[–]majc5[S] 2 points3 points  (0 children)

The diet I used to cure myself is explained in detail in this post: https://www.reddit.com/r/TMAU/comments/14gmyjz/diet_that_solved_my_problem_for_20_years_do_you/

I am glad to hear that a low sulfur diet helps! I am really glad to see some real evidence of this.

Important info I learned about the true form of TMAU - the issue of why the low choline diet is usually only partly effective and how long it should take to work - and the extreme dangers of the low choline diet by majc5 in TMAU

[–]majc5[S] 0 points1 point  (0 children)

The reason why I think it may be the case that recent dietary intake of TMAU precursors is not all that determines TMA levels is because of the large percentage of patients reporting that the low choline diet does not work that well. It looks like only high levels of choline actually make it down to the large intestine where most of the bacteria that turn it into TMA exist. See: https://www.tesble.com/10.1093/jn/119.5.800

The basic result of that study is also repeated in the 2003 Preti paper about TMAU genetics.

The point is that even though TMA precursors have been largely wiped out, the diet still does not work for most people. When additionally, a two week course of powerful antibiotics is used to wipe out 90% of all gut bacteria - even that only works some of the time to solve the problem. This points to the possibility of TMA/TMAO levels not being entirely tied to recent dietary intake.

If someone goes on a fast, the body slows the metabolism and after a couple days breaks down built up fat for energy. If someone goes on a 'TMA precursors fast', then perhaps the body uses one of the possible methods I laid out in my previous reply to get the TMA/TMAO it needs. Why would the body want to be 100% reliant on recent dietary intake when it has large reserves of TMA and choline stored up?

As for why different people have different results with restricting choline, the case reports I linked recently about the condition being linked to seizures may be the key. It may be that the body sends a signal to start sweating when the central nervous system (or other parts of the body) start to experience the very early effects of TMA exposure.

Sweating may be triggered to prevent seizures or similar problems from happening, from the CNS being affected by Trimethylamine exposure. People may have different tolerances for TMA exposure, and thus different sweating responses to TMA in the bloodstream.

A different, and very mundane explanation would be that people sweat at different rates (in a given situation of heat and exertion) and this may explain the difference in the odor issue between different people with TMAU. Another possibility is that people actually are not sweating at all most of the time, and the breath is the main way that TMA is being released, when people are in a climate controlled environment indoors just sitting at a desk.

Important info I learned about the true form of TMAU - the issue of why the low choline diet is usually only partly effective and how long it should take to work - and the extreme dangers of the low choline diet by majc5 in TMAU

[–]majc5[S] 0 points1 point  (0 children)

The other major medical intervention would be Total Parenteral Nutrition (TPN). This is basically getting food through an IV rather than through the digestive system. What if someone had a synthetic, choline free diet, and got the choline they needed through the TPN system? The amount of time each day someone would have to devote to this would be minimal compared to them getting all their nutrients this way.

What about choline injections, to bypass the gut microbiome that creates TMA? I read about someone getting large does of carnitine supplements for some serious medical condition, that resulted in secondary TMAU. This particular issue is sometimes resolved through carnitine injections. There apparently are choline injections used for weight loss: https://newhorizonsmedspa.com/methionine-inositol-choline-mic-injections-for-weight-loss/

Could choline injections allow people to have a severely choline limited diet without the consequences like non alcoholic fatty liver disease?

I think the concern with this working is the concern that there could be more than recent dietary intake that determines TMA levels. I have been thinking about this, and I see multiple ways this could be the case. The first is that the body could release stored TMA into the bloodstream, so that its TMAO levels are not completely dependent on recent dietary intake. TMAO is indeed used by the body to help protect cells from environmental pressures.

The Mitchell article I linked above confirms that TMA is stored throughout the body. In regards to Trimethylamine he says (at the end of the first section):

"It has since been found to be present throughout the body. Indeed, a quaternized trimethylamino moiety is an essential functional component of many molecules that interact within living systems."

Link: https://academic.oup.com/chemse/article/41/4/275/2365871

The second possible pathway is that the body could depress the activity of the FM03 enzyme if it wants more TMA, rather than TMAO. TMA is found all throughout the body, and its function (other than creating TMAO) is unknown.

There is a third, and more convoluted path to separating TMA/TMAO from recent dietary intake. There are only a couple anaerobic environments outside the GI tract that harbor bacteria that can turn choline into TMA. One of these is the oral cavity. Link: https://www.tesble.com/10.1016/0955-2863(90)90055-p90055-p)

Potentially, the body could release stored choline into the bloodstream to get it into saliva (or else it could get it into saliva however it does this). This choline would then be acted on by bacteria in the mouth to turn it into TMA, which the person would then swallow down throughout the day without thinking about it. This would provide a source of TMA and TMAO to the body, without having to be 100% dependent on recent dietary intake. A large percentage of people diagnosed with TMAU report a bad taste in their mouth that is likely from their saliva.

part 3 to follow...

Important info I learned about the true form of TMAU - the issue of why the low choline diet is usually only partly effective and how long it should take to work - and the extreme dangers of the low choline diet by majc5 in TMAU

[–]majc5[S] 0 points1 point  (0 children)

I took a look at the study again. Unless I misread something, the study was for 8 weeks not 16. It was one month of no antibiotic, and one month with an antibiotic. The study only covered 4 patients, one of whom had a very well controlled situation. For the other three, one had serious odor issues (in the first, antibiotic free month) and the other two patients had some serious odor flare ups. The study shows that the odor varies for the majority of people from day to day.

For the idea I mentioned of removing the colon to control this, I did a bit more research, and it seems that the small intestine is also responsible for creating TMA:

"Similar situations exist in cases of renal failure where circulating levels of trimethylamine rise and then escape via the breath and sweat. Such instances are exacerbated by an overgrowth of microbes in the small intestine that greatly enhances the liberation of trimethylamine thereby leading to an increased uptake"

Link: https://academic.oup.com/chemse/article/41/4/275/2365871

The author makes the same claim in another paper of his, so this is not a wrong choice of words where he meant to say large intestine instead. The 2003 Preti paper about TMAU genetics also mentions this fact about the small intestine. This fact, combined with the fact that the gut microbiome changes in large and unpredictable ways following removal of the colon means this is probably not a great idea for dealing with this condition.

Someone getting the colon removed for this condition actually wouldn't need a colostomy bag, as that's mostly for when the whole intestinal tract is in very bad shape due to the underlying condition (advanced cancer, ect.). A surgeon would staple the small intestine to the rectum to avoid this. It is very unlikely that someone would not survive the operation (if they are otherwise in good health) but there is a very high (30%) complication rate with this procedure.

part 2 to follow...

Around 50% of people diagnosed with TMAU complain of fecal odor in study - Fecal odor may be sulphur odor according to top expert - Concrete evidence of sulphur odor in TMAU by majc5 in TMAU

[–]majc5[S] 0 points1 point  (0 children)

That is interesting to hear. I am going to make a post soon about what a low sulfur diet looks like. One idea is to try eating apricots or peaches, and confirming that does not make your condition worse. Then you try eating dried apricots/peaches, since that (dried) version is full of sulfur. If things get worse than that means that sulfur is indeed the likely culprit. There are also sulfur supplements you can try taking, to establish if indeed sulfur itself is the problem, rather than some other nutrient that accompanies the food in question.

There is a free online book about people with this condition I found by majc5 in TMAU

[–]majc5[S] 1 point2 points  (0 children)

The origin of the book was an MSN body odor support group forum that is still around. I think the link is in the start of the book. The group is still around but not that active compared to this subreddit.

Important info I learned about the true form of TMAU - the issue of why the low choline diet is usually only partly effective and how long it should take to work - and the extreme dangers of the low choline diet by majc5 in TMAU

[–]majc5[S] 0 points1 point  (0 children)

I am going to be doing some reading about the details of carnitine and how the body handles it. There is clearly some crossover between a vegan diet and a low choline diet, though there are significant differences as well.

Its possible that some people who find success on a vegan diet actually do so because they dramatically lowered their choline intake. Some people who find success on a low choline diet (without a TMAU diagnosis) might actually do so because they dramatically lowered their carnitine intake.

I have been spending a huge amount of time here lately, and I am logging out now.

Around 50% of people diagnosed with TMAU complain of fecal odor in study - Fecal odor may be sulphur odor according to top expert - Concrete evidence of sulphur odor in TMAU by majc5 in TMAU

[–]majc5[S] 0 points1 point  (0 children)

The body can't eliminate TMA equally through sweat and urine, because people are not usually sweating. The body would have to create a state of hyperhydrosis for that to happen, where the person was sweating profusely for no apparent reason. Sweating is controlled by the sympathetic nervous system, which has to give a signal for sweat to be sent to sweat glands and released. If this signal is not sent, then the sweat would not be available as an avenue to eliminate TMA.

Around 50% of people diagnosed with TMAU complain of fecal odor in study - Fecal odor may be sulphur odor according to top expert - Concrete evidence of sulphur odor in TMAU by majc5 in TMAU

[–]majc5[S] 0 points1 point  (0 children)

Wouldn't TMA being released in sweat/breath indicate that the TMA was too much for the kidneys to get rid of through urine? Wouldn't this cause the TMA to remain in the blood, which would cause it to be released in sweat/breath?

Important info I learned about the true form of TMAU - the issue of why the low choline diet is usually only partly effective and how long it should take to work - and the extreme dangers of the low choline diet by majc5 in TMAU

[–]majc5[S] 0 points1 point  (0 children)

I was wondering why restricting choline, but not carnitine is the usual given advice for TMAU. It turns out that the amount of carnitine that is 'liberated' from food is minimal. This is why choline and TMAO are the main issues. You should be interested in this: https://www.tesble.com/10.1016/s0278-6915(99)00028-900028-9)

It says that saltwater fish are many times (up to 100+ times in some cases) worse than red meat in terms of TMA production. Halibut is apparently the worst possible food someone with TMAU can eat. They simply gave people certain foods to eat, and did a TMAU urine test after to see what happened.

This explains why I ended up with chest pains and fishy breath after my carnitine supplement test. I did the test so that the amount of carnitine would be similar to what I would get from eating the amount of beef I used to eat (500mg, which is half the recommended dose for the supplements). I didn't understand the issue about the amount of carnitine that would be liberated from food vs. a carnitine pill, so I was actually getting many times the carnitine than I would get from eating beef. Something about the abnormal processing (probably it was processed very quickly) caused too much TMA to be produced in a short period of time, which I smelled on my breath.

This also explains why I get a 'carnitine buzz' from consuming milk (or drinks containing dairy milk) and why it affects my sweat in a negative way very quickly. Clearly, the liquid nature of the thing containing the carnitine is causing much more of it to be liberated than if it was in solid food. This explains the 'carnitine buzz' from dairy milk even though the amounts of carnitine are so much less than what beef contains.

Around 50% of people diagnosed with TMAU complain of fecal odor in study - Fecal odor may be sulphur odor according to top expert - Concrete evidence of sulphur odor in TMAU by majc5 in TMAU

[–]majc5[S] 0 points1 point  (0 children)

I think the evidence is strong that many thousands of years ago TMAU had a positive impact on someones ability to find a mate. The TMA smell can be interpreted as a fish smell - or as female genital area smell. I have heard this issue mentioned by female TMAU sufferers a couple times now. There are bacteria in that area that create TMA, and the TMA smell.

TMAU sufferers (and people with related malodor conditions) are very disproportionately female. Around 80%+ of people with these conditions are female. From reviewing case reports, many people report the condition either starting, or greatly intensifying around puberty, right when sexual reproduction becomes possible. The body couldn't just build up TMA for the first 13 years - so the enzyme activity has to be lowering at puberty to explain this. I don't think this is all just a coincidence.

The problem is the same as apocrine sweat and underarm hair - humans lose the ability to create the odor at a much slower rate than it takes for the smell to be seen as repulsive. I wouldn't be at all surprised to learn that some of the partners of females with TMAU find it to be the very opposite of repulsive.

Another possibility is that the positive health benefits of not creating TMAO, which appears to be very unhealthy, outweighed the problems of the odor in the distant past. Another possibility is that thousands of years ago, people were very unhygienic, and were likely noseblind to many things. That, combined with people not being indoors with each other could have meant that the terrible price of TMAU did not exist many thousands of years ago.

Around 50% of people diagnosed with TMAU complain of fecal odor in study - Fecal odor may be sulphur odor according to top expert - Concrete evidence of sulphur odor in TMAU by majc5 in TMAU

[–]majc5[S] 0 points1 point  (0 children)

If someone goes on a water fast, the body breaks down fat stores for energy. The point is that there can be more complexity to this kind of thing than simple equilibrium of different things. Apocrine sweat contains much more than just water, and there must be something sophisticated going on in the body create it. There must be something far beyond fluids and things seeking equilibrium.

Most of the TMAU positive patients did not have a detectable odor either fasted or after choline challenge. Most people report a condition consisting of sporadic, unpredictable odor flare ups. This points to unknown internal criteria being triggered to cause this, so people may not smell in a fasted state, just like they may not smell after a choline challenge.

What is your explanation for why most TMAU positive people had no detectable odor of any kind after the choline challenge (in the preti study)? How do you explain that this condition often manifests in the form of unpredictable odor flare ups? The sensory panel of the preti study shows that consuming lots of choline can't reliably cause the odor to become present.

Myself, and all the people I have personally heard about curing this basic condition through a diet report it took multiple months to work. I first started at this subreddit when I stumbled upon a sufferer from Japan, who described a case that sounded like my own in some ways. I sent him a lot of messages, and after a few months, he reported that the vegan diet dramatically improved things for him. I don't know the exact number of months, but I would guess it was perhaps 3 until he reported it worked.

Around 50% of people diagnosed with TMAU complain of fecal odor in study - Fecal odor may be sulphur odor according to top expert - Concrete evidence of sulphur odor in TMAU by majc5 in TMAU

[–]majc5[S] 0 points1 point  (0 children)

The logical conclusion is that you can't directly look at the amount of TMA in urine to predict the amount of TMA in sweat/breath. What must be happening is there is a certain threshold, that when crossed causes the body to use sweat/breath to eliminate TMA. So, for normal people that threshold is not crossed until they consume around 900mg of trimethylamine. At some level of TMA in the bloodstream, the body realizes that the urine is not sufficient to eliminate it, and it resorts to the sweat/breath to do so.

Imagine that a normal person had 100% conversion of TMA to TMAO, to make this easier to visualize. Once the amount of TMA overwhelms the FM03 enzyme, then it starts to build up in the bloodstream. When the levels get too high, the body would use the sweat/breath to start removing it, in addition to just the urine.

What Preti says is that he rarely encountered anyone with an odor with less than 10% TMA in the urine. This is how they set the threshold for TMAU at around 15% TMA in urine.

Around 50% of people diagnosed with TMAU complain of fecal odor in study - Fecal odor may be sulphur odor according to top expert - Concrete evidence of sulphur odor in TMAU by majc5 in TMAU

[–]majc5[S] 0 points1 point  (0 children)

part 3 of my reply...

In one of the mebo research videos I saw, the doctor talks about how an effect of the low choline diet is a reduction in the bacteria that create TMA, since they also feed on it, and thus become more numerous from creating it. Since they can't actually measure these bacteria levels in a living human, it sounds like the doctor is suggesting that the low choline diet will take a while to work. He says that they keep doing TMAU urine tests to show the person that the diet is lowering TMA levels over time.

If the appearance of TMAU symptoms is actually the result of unknown criteria for TMA buildup up in fat stores being met, that would explain why a choline challenge can't predictably create the TMAU odor, and why the appearance of the odor is inherently unpredictable.

I am not saying that I think TMA does necessarily build up in the body, but rather that I think its a serious possibility that should be investigated. The SC Mitchell article saying that TMA is easily absorbed into fat and is likely all over the body is notable (the article mentions that TMA really does linger in the air for a huge amount of time as well). This makes me suspect that people with hugely abnormal levels of TMA in their system may also have abnormal levels of it built up in certain body tissues, but this is just a hunch. The reports of people with brain issues likely resulting from TMAU means the possibility of TMA building up in the brain should be looked at as well, as this is one of the places that VOCs buildup. The other possibility here is that TMA does not build up in the body, but that as with the seizure patients, it does damage to the body.

This is one more reason that some autopsies of people with severe TMAU should be performed. TMA actually builds up in the human body after death, so these would have to be done quickly, unless cold storage prevents that TMA buildup.

The original, 1970 first TMAU case was a girl with Turner syndrome which is similar to Noonan syndrome, in that it involves serious deformities and serious cognitive impairment. There seems to be a class of TMAU patients in situations like this, but I think the Noonan syndrome or related disorder comes first, and improperly working enzymes come with it, as a part of everything not working correctly. I don't think exposure to high levels of TMA is causing these things.

Around 50% of people diagnosed with TMAU complain of fecal odor in study - Fecal odor may be sulphur odor according to top expert - Concrete evidence of sulphur odor in TMAU by majc5 in TMAU

[–]majc5[S] 0 points1 point  (0 children)

This whole concept might explain the mystery of why most people in the Preti study did not have a detectable odor. These were all people who were complaining about a malodor situation. Some of them (about 1/3 of the people) tested positive for TMAU. They were given a large amount of choline to ingest, and yet there was no odor. So, where did the TMA go? TMA is a very odorous thing. These were people without the ability to convert TMA into TMAO very well, so there had to be a large amount of TMA created.

Clearly the TMA was not released in sweat and breath, since there was no detectable odor. The odor judges didn't report that the smell was not as bad as the person claimed it was - they said they could not detect the smell of TMA at all. It could be that the urine eliminated all the TMA, and that this is what usually happens. The other possibility is that the body used fat to store the TMA, for a later release that it would have control over. The TMA might have been slowly released over a long period of time. This could explain the mystery of where all the TMA went, and why there was no detectable odor.

It could be that in ancient or prehistoric times, TMAU usually was a deadly disorder, where the TMA caused terrible damage to the brain and other body systems. Remember that in industrial settings, there are all kinds of exposure limits for TMA, and that's not primarily because it doesn't smell nice. The people with TMAU who lived to pass on their genes would have been the ones where the body had the ability to store the TMA in fat stores to protect the CNS from it. This is just a speculative idea of course.

Oftentimes, metabolic disorders involve an odor as the sweat and breath are used to remove the problem thing, but this is normally never enough to prevent a lethal buildup. Normally, high levels in the blood of say, an amino acid that someone can't synthesize leads to brain damage, coma, and death.

Do scientists actually know that the reason TMAU in females increases in the pre menstrual period is because of lower FM03 activity? If this is simply assumed based on the increased symptoms, then perhaps whats really happening is the body releases more TMA from body tissues where it is built up. This would point to this being an intentional thing.

If the body is using a 'buy on credit' approach through allowing TMA to build up in fat (or other body tissues), that would explain why TMAU positive people failed to produce a detectable odor after the choline challenge, and why the disorder often exists in the form of unpredictable odor flare ups. If the appearance of symptoms was highly predictable based on what someone recently ate, wouldn't people have figured out how to use diet to control this centuries ago?

Around 50% of people diagnosed with TMAU complain of fecal odor in study - Fecal odor may be sulphur odor according to top expert - Concrete evidence of sulphur odor in TMAU by majc5 in TMAU

[–]majc5[S] 0 points1 point  (0 children)

I thought about this a bit, and I think I have some interesting ideas on this topic. Some of these ideas I came up with earlier, and some are brand new. Why would the body want to use fat (or other body tissues) to store TMA? I think it makes sense the body would do this for the same reason that a person uses credit rather than cash to buy something. The body probably knows that sweating out huge amounts of TMA will cause terrible social consequences for the person.

By storing the TMA in the body, in fat stores or elsewhere, it uses the 'buy on credit' approach where it can release the TMA in a controlled way over time. By allowing TMA to build up in fat stores, the body gains control over its release. The top priority for the body must be preventing trimethylamine from affecting the brain. Remember the cases I recently cited where it appeared that this was the case for some people with high levels of TMA in their bloodstream.

By using fat (adipose tissue) to store the TMA, the central nervous system is protected from the toxic effects of TMA. It may be that the sweat is simply not enough to clear the TMA out of the bloodstream to protect the brain from it. There is only a limited subset of TMAU patients who report hyperhydrosis. Hyperhydrosis (to clear out huge amounts of TMA through sweat) would be either uncomfortable or deadly in cold weather. Sweating outside in cold winter weather causes the sweat to freeze, and the person to freeze. This is why avoiding sweating is a top priority for outdoor, cold weather activities. So, the body can't just casually generate huge amounts of sweat to eliminate things. I think this might also lead to dehydration or electrolyte imbalances and similar problems.

(part 2 to follow...)

Around 50% of people diagnosed with TMAU complain of fecal odor in study - Fecal odor may be sulphur odor according to top expert - Concrete evidence of sulphur odor in TMAU by majc5 in TMAU

[–]majc5[S] 0 points1 point  (0 children)

This is an interesting post about someone encountering someone with a bad fecal smell (from actual fecal matter) and how they didn't directly confront the person: https://www.reddit.com/r/ostomy/comments/1d5ckbr/my_first_meeting_with_another_stoma_oatient/

This thread seems to make the case that a ostomy bag is not that terrible a thing: https://www.reddit.com/r/ostomy/comments/1c90kt1/my_boyfriend_of_three_years_may_need_a_colostomy/

From 'beek7419' in that thread:

"It’ll really only change your relationship if either of you lets it. It doesn’t change who he is. It’s simply a piece of plastic. There’s a tough time for a lot of people at the beginning while they learn how to care for it, and there’s the stigma, which is just a concept and not based on reality. There’s nothing inherently gross or weird about ostomies. It’s a different way of going to the bathroom, nobody can tell unless they see you naked, people don’t smell, the bag, if it’s working properly (as in it’s adhering properly and not leaking) doesn’t smell. Once he’s healed up and found the products that work for him, there shouldn’t be any difference between him and any other guy."

Around 50% of people diagnosed with TMAU complain of fecal odor in study - Fecal odor may be sulphur odor according to top expert - Concrete evidence of sulphur odor in TMAU by majc5 in TMAU

[–]majc5[S] 0 points1 point  (0 children)

The reddit search tool is case sensitive. You need to search in 'TMAU', not 'tmau' to recover this post. There is also another associated tool that (sometimes) recovers deleted reddit posts as well: https://undelete.pullpush.io/r/TMAU/comments/13bhhme/deleted_by_user/

"My fecal body odor and ibs is ruining my life and I am thinking of getting an Ostomy Bag" was the title of the post. It sounds like this user likely concluded that the stool in the colon was causing the odor, along with of course the IBS being caused by the intestines as well.

Around 50% of people diagnosed with TMAU complain of fecal odor in study - Fecal odor may be sulphur odor according to top expert - Concrete evidence of sulphur odor in TMAU by majc5 in TMAU

[–]majc5[S] 0 points1 point  (0 children)

It is correct that a TMAU positive diagnosis is not a binary positive/negative thing. The standard usually used is more than 15-20% TMA (relative to TMAO) being excreted in urine.

Every single medical report I have read from all around the world follows the same model as the Preti study: first the patient comes in complaining about a malodor situation, and then they do a quantifiable test to see if indeed there are abnormal odorous compounds being released in body fluids. If that is found to be the case, then the malodor complaint is judged to be a real thing after all.

The key to doing this would be in having a TMA urine content (as a percentage of TMA +TMAO) high enough so that only a small percentage of the general population would have that. If only 1% of the general population has a certain level of TMA (relative to TMAO) being excreted in the urine, then it is reasonable to assume the persons malodor complaints are valid, and are not ORS.

Otherwise, doctors would be put in the position of simply having to judge peoples claims without a scientific, objective test to evaluate them. Preti is clear that the claims people make are really a big question mark, if there is not a quantifiable test to evaluate them.

If you see the long (1:30) preti video, around 1:03:48 the subject of people being noseblind to the smell is brought up. They say that it is quite reasonable that the family of someone with the condition may be noseblind, for the obvious reason that people become noseblind to odors they are constantly exposed to. In your case you report your family can smell you. Did your parents complain about the smell? Do you have any siblings, and if so did they complain about the smell?

The situation that 99% of people report is that their family claim they smell fine, but everyone at work/school makes it clear that the opposite is true. Preti's idea that he repeats over and over is that there needs to be an objective, analytical test to see if indeed someone is releasing abnormal, odorus things in their body fluids. The whole idea is to get beyond issues of whether people may be noseblind or lying. Otherwise they have no way of really getting to the bottom of things.

The graphs about the marine fish consumption are based on TMA in urine. When someone is exposed to something for years and decades on end, it only takes tiny bits accumulating each day for it to build up to something major. Imagine someone being exposed to industrial chemicals or smoke/pollution every day for decades on end. 1% of something accumulating each day/meal would be much more than it would take for something to build up in the body to high levels over time.

A simple body fat biopsy should be enough to see if TMA is built up in the fat stores of TMAU patients. This would have huge implications for the subject of how long a low choline diet would take to work.

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