Haloscan comment system closing down

 

Haloscan comment system closing down

The comment system we use for the blog, Haloscan, is closing down on the 30th December. We have exported all the comments and hope to import them into the new comment system we will use, the default system in blogger. Haloscan was never a perfect choice, but was chosen for (perceived) privacy concerns. Thank you to everyone who has posted a comment and we hope the transition to the default system goes smoothly.

Update : the blogger default comment system is now in place and seems to be functioning correctly. People can post anonymously, although all posts will be premoderated so as to avoid spam and any offence (since it's such a sensitive subject). Previously it wasn't possible to premoderate blogger comments, which is a main reason Haloscan was originally chosen.

Editor's Note (2026):

This post was originally written by blogcontributor2, one of MEBO Blog admins, in 2009, when the Haloscan commenting system was closing down. While the Haloscan name still exists in various forms today, it is no longer the same service or community platform that many blogs relied upon at the time.

Recovering this post is also a reminder of how easily knowledge disappears on the Internet. Websites close, domains change hands, commenting systems are retired, and valuable discussions quietly vanish. Patient communities are particularly vulnerable because much of their experience is shared through small websites, forums and blogs that were never archived properly.

The original MEBO website suffered a similar fate when the domain changed ownership and the blog was no longer connected, leaving years of posts effectively hidden from readers. As part of rebuilding the archive, we are restoring these articles so that the information - and the history of the TMAU community—is not lost.

Not every old idea remains current, and some scientific understanding has evolved since these posts were first published. However, preserving them provides a valuable record of how knowledge, patient experiences, and research have developed over time.

Different outcomes of TMAU urine test

 

A UK volunteer does the TMAU urine test twice and gets different outcomes

TMAU urine test results of a UK volunteer

	Jan 2009	Sep 2009	Ref. range
Urine creatinine	5.5	4.0
Trimethylamine(TMA)	56.8	32.1	2.5 - 10.9
TMA-n-Oxide	719.3	78.0	17.0 -147.0
TMA/TMA-n-Oxide	0.08	0.41	0.05-0.21

• The first sample taken in January 2009 was done with a choline food load and while directly pre-menstrual.
• The second sample taken in September 2009 was done WITHOUT a choline load and while NOT pre-menstrual.
• The tester had been following the low-choline diet between the two tests.
• The conclusions were 'secondary TMAU' in the first test, and 'primary TMAU' in the 2nd
  
• This tester is now having the gene blood test done this week. Results will be forthcoming and posted in this blog.
• Note: TMA is trimethylamine. Trimethylamine-n-oxide is the odorless metabolised end product. It is known as TMO or TMAO or TMA-n-O
  

A member of our community has kindly given permission to post her TMAU results in the blog in order to promote discussion on the current test protocol in various countries (there is no international agreed standard). These results are from the UK, and so from Sheffield Hospital, which is the only clinical tester in the UK. The parameters used were described by the tester Nigel Manning in a previous post:

TMA is regarded as normal if the concentration is below 11 micromoles per millimole of creatinine. TMA-oxide’s normal range is below 147 and the ratio of TMA to TMO is normal below 0.21.
SecondaryTMAU is a very broad term, but essentially relates to any TMAU where normal TMA oxidation appears to be indicated. Increased TMA and TMO are usually markers for TMAU2...

Nigel Manning TMAU interview

In simpler terms, Primary TMAU is a reflection of a subnormal level of conversion of TMA to TMA-n-oxide (lower than normal TMA-n-oxide production is representative of Primary TMAU). Regardless of the TMAO level, Secondary TMAU is deemed as an excessive level of TMA even if the TMA/TMAO ration is within normal limits.

In this case, while taking high choline foods, the first test shows a very high level of TMA, but her FMO3 enzyme was able to oxidize the vast majority of it, and therefore, the ratio was very low/normal. Nevertheless, the TMA present was well beyond the 'normal' range, so she was deemed as having 'Secondary TMAU' as a result.

To further confuse things, Nigel Manning mentions that he has seen cases where someone diagnosed with 'primary TMAU' (including genetic diagnosis) can later be shown to have normal levels of TMA-oxide in a later test (this should be impossible if you have genetic primary TMAU). This seems to be what is shown here. Presumably it is unknown why this is (most likely due to lack of interest from the research community)

Quote from Nigel Manning:

SecondaryTMAU is a very broad term, but essentially relates to any TMAU where normal TMA oxidation appears to be indicated. Increased TMA and TMO are usually markers for TMAU2, however we have seen TMAU1 patients (with proven FMO3 enzyme deficiency by DNA mutation analysis) whose samples also showed this pattern – albeit only temporarily. This makes the differentiation between TMAU1 and TMAU2 difficult without more than one sample to assess and without DNA analysis to confirm a mutation for the FMO3 gene.
In general – if the TMA is consistently increased the patient has TMAU.

Interestingly, in the 2nd test results where the low choline diet had been followed, the outcome diagnosis based on the 'ratio' was 'Primary and Secondary TMAU'. Her TMA level was still too high (secondary TMAU) and her TMA-oxide level was still within normal range, but according to Nigel Manning's ratio she is deemed as not converting the TMA to TMAO to a 'normal' level.

It is unclear if this particular ratio is used elsewhere. There has been mention of a different ratio used in the USA, the percentage of free TMA in regards to the whole TMA and TMAO output : TMA / TMAO + TMA.

The paper by Phillips and Shephard that is used on the NIH website describes the ratio as :

Primary TMAU parameters:

Percent of total trimethylamine (TMA) (i.e., free TMA plus the non-odorous metabolite TMA N-oxide) excreted in the urine as unmetabolized free TMA

• Severe trimethylaminuria: less than 40% of total TMA excreted as unmetabolized free TMA
• Mild trimethylaminuria: 10%-39% of total TMA excreted as unmetabolized free TMA
• Unaffected: 0%-9% of total TMA excreted as unmetabolized free TMA

NIH Trimethylaminuria explanation

It seems that whether using the percentage or Nigel Manning's ratio, both would have concluded roughly the same result here. Her percentages would have been 92.7% normal and 70.9%.

There is a pubmed paper that suggests menstruation could cause someone to be temporarily 'Primary TMAU', even if they are regarded only as a 'carrier' (of a FMO3 mutation). Perhaps the hormones have an inhibiting role on FMO3.

In comparison, three healthy control subjects that harbored heterozygous polymorphisms for [Glu158Lys; Glu308Gly] FMO3 or homozygous for wild FMO3 showed normal (> 90%) metabolic capacity, however, on days around menstruation the FMO3 metabolic capacity was decreased to ~60–70%.

Paper : Transient trimethylaminuria related to menstruation

In a citation paper done in 2008 regarding people who had been deemed 'primary TMAU' by the urine test, the citation went on to DNA test the 12 samples and only 4 were deemed 'genetically proven primary TMAU'.

In a set of our patients, two deleterious mutations were identified in 4/12 patients including a novel T237P sequence variant, while the majority of our patients (8/12) did not reveal any mutations. Some of the latter were double heterozygous for the E158K and E308G polymorphisms which could explain a mild phenotype while others had only the E158K variant which raised the question of undetected mutations. These results indicate that further experiments are needed to further delineate the full mutational spectrum of the FMO3 gene.

Genotypic spectrum and genotype-phenotype correlation of trimethylaminuria

Probably the only conclusion that can be currently made is that it is by no means a completely defined disorder and much more research is needed into trimethylaminuria. Those that can afford the test, it is perhaps best to do the urine test a few times to make sure, and the DNA test once.

Human olfactory psychophysics

 

Wednesday, June 3, 2009

Human olfactory psychophysics

This is a mainstream research paper about the sense of smell and is probably the current viewpoint of the mainstream on the olfactory system. It mentions concepts such as 'specific anosmia', 'threshold', and 'adaptation'. 'Specific anosmia' is the genetic inability to smell specific smells. Fecal body odor sufferers (or other bowel smells or other odd smells) often say they cannot smell themselves. This also seems to be the general rule for people with external body odor. However, those with fecal body odor can smell feces odor from other sources (not through human skin, it seems), so specific anosmia doesn't seem to be the reason. The same seems true for trimethylaminuria and probably other metabolic body odors, although Dr John Cashman believes that perhaps 8% cannot smell trimethylamine, although it's not known if he means only from humans or from any source. for example, most people seem to be able to smell fish. Another theory for this is 'adaptation' and desensitivity to the smell. This seems more likely than specific anosmia, however, perhaps sufferers have been in situations where a group of strangers complain of a smell but one stranger says they can't smell anything (for instance in school). Adaptation and desensitivity do not seem to account for this. At the moment it is a mystery. the most likely guess is that there is some genetic aspect, as of yet unknown.

That aside, the article is seemingly the 'latest' (2004) in olfactory perception and worth a read

Human olfactory psychophysics
Andreas Kellera and Leslie B. Vosshall 2004

Part 2 of interview with Cass Nelson-Dooley of Metametrix

Tuesday, March 24, 2009

The following is Part 2 of the interview with Cass Nelson-Dooley, Clinical Consultant at Metametrix, with contributions by Mr. Tony Hoffman

Part 1 can be read here

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Gut-smells body odor

Are you amazed that there are people around who smell of gut smells?

Yes, I imagine that must be difficult to deal with. I would compare it to the example of eating garlic. The sulfur compounds from garlic are liberated by chopping and chewing and these sulfur compounds emanate from the mouth and even the skin for some time afterward.

What causes fecal smells? (i.e. what does feces actually smell of and why)

The smell of feces comes from short chain fatty acids (SCFAs) and bacteria like E. coli. All the SCFAs have strong smells. Butyric acid is an SCFA and it smells like feces and even like body odor. E .coli has more of a mousy odor.

Do you have a good idea what microbes in particular cause gas smells? Do you have any theories as to how someone could smell of gut smells through their pores/breath?

It is likely that bacterial overgrowth occurs in the small bowel and the products are absorbed and then emanate from the skin. I wouldn’t expect that the malodorous products would be absorbed from the colon. If someone has an overgrowth of Disulfovibrio, there may be a sulfur smell. If someone has an overgrowth of Pseudomonas sp., the smell may be sweeter (grape-like), but still sickly sweet. There is a whole group of sulfur-producing bacteria. Citrobacter freundii produces sulfur. Additionally, if the person suffers with maldigestion then food will undergo fermentation and this produces putrefactive compounds such as putrescine. While blood borne body odor is likely multi-factorial, at least for some patients, healing the bowel and cleaning up the diet could provide some relief.

Do you think with gut-related metabolic body odors, it's likely an enzyme is saturated? For instance a drug metabolizing enzyme? Any thoughts as to which one(s)? Any thoughts as to a scenario?

In addition to dysbiosis, I think it could be enzyme saturation or lack of vitamin and mineral cofactors. Metabolic diseases such as amino acidurias or organic acidurias have been characterized by strange odors, especially in the urine. These disorders occur due to lack of an enzyme, poor function of an enzyme, or low levels of cofactors causing the enzyme to malfunction. The result is too much of the byproducts, which can be smelly in high concentrations.

Does leaky gut mean 'leaky small intestine'? Do you think leaky gut or 'leaky colon' is likely a factor?

Leaky gut is often involved in cases of dysbiosis. It could be a factor in people with blood borne body odor, but I wouldn’t know for sure without an IgG4 food antibody test. Intestinal permeability, or “leaky gut,” has been implicated in inflammatory bowel diseases such as Crohn’s disease, non-alcoholic fatty liver disease, alcoholic liver disease, food allergy, acute pancreatitis, celiac disease, multi-organ dysfunction, and autism. According to the leaky gut hypothesis, genetic predisposition to poor intestinal barrier function, coupled with stressors such as NSAIDS or alcohol, can result in permeation of the intestinal mucosa. Antigens and bacteria are then able to cross the intestinal membrane and enter circulation where the immune system launches an attack against the antigens.

What kinds of tests would you recommend for a person suffering with blood borne body odor?

Without knowing a detailed history on the patient, I would recommend the GI Effects, the Organix, and the 40 amino acids. I recommend those lab tests because of the likely involvement of gut dysbiosis and abnormal SCFAs, vitamin need, and metabolic diseases involving amino acids and organic acids. I would also recommend IgG4 Food Antibody testing, especially if the person has gut, skin, or autoimmune symptoms.

Trimethylaminuria

Do you think a particular type of bacteria are responsible for gut trimethylamine production? Is it likely the same one thought to cause bacterial vaginosis (Gardnerella)?

Yes. The more smelly compounds like trimethylamine and hydrogen sulfide are not products of human metabolism, but they are produced by several bacteria under certain conditions. They tend to be strict anaerobes that could dwell in the colon or the vagina.

There is a 'diagnosis' of 'Secondary TMAU', where the enzyme involved is deemed fine, but the person has too much trimethylamine. Do you have any suggestion as to how to kill off the TMA-producing bacteria in particular?

The first thing to do is lower protein intake and improve protein digestion to reduce undigested nitrogenous substrates (amino acids) that must be present to form ammonia. Perhaps water or juice fasting could be beneficial in these instances as it can change the microbial content of the gut. If you don’t feed the colonic bacteria, they can’t grow and produce strange products.

Some feel that trimethylamine can produce a wide range of odors. Do you think trimethylamine could cause the wide range of gut smells on its own?

No. However it can be a component in complex mixtures of products that are responsible for the varying odors among individuals.

Final Questions

What do you think of the quality of probiotics on the market and are there any brands of probiotics you recommend ?

We are impressed with Klaire Labs probiotic and prebiotic formulas. I also like Custom Probiotics and a high dose probiotic called VSL#3. Designs for Health has a good probiotic product as well.

Is taking prebiotics on its own a good idea ? And which type of prebiotic do you feel is best ?

Fruits and vegetables are a great source of fiber (prebiotics). Other ideas are inulin, xylooligosaccharides, larch arabinogalactans, and beta glucan.

Is there general treatment advice for 'suspected' dysbiosis or does it vary too much ? For instance, take nystatin and metronidazole in a 'scorched earth' policy ?

I think the “4R Protocol” is the most general treatment advice and it’s comprehensive, but every doctor has a different approach and dysbiosis treatment should be tailored to the patient.

Treatment using 4 “R” Protocol for Intestinal Health from the GI Effects Interpretive Guide

Remove offending foods, medications, gluten (if sensitive) and reduce poor quality fats, refined carbohydrates, sugars, and fermented foods (if yeast is present). Consider antimicrobial, antifungal, and/or antiparasitic therapies in the case of opportunistic/pathogenic bacterial, yeast, and/or parasite overgrowth (see below for specific recommendations).
Replace what is needed for normal digestion and absorption such as betaine HCl, pancreatic enzymes, herbs that aid in digestion such as deglycyrrhizinated licorice and marshmallow root, dietary fiber, and water.
Reinoculate with favorable microbes (probiotics such as Lactobacillus sp., Bifidobacter sp., and Saccharomyces boulardii). To enhance the growth of the favorable bacteria, supplement with prebiotics such as inulin, xylooligosaccharides, larch arabinogalactans, beta glucan, and fiber.
Repair mucosal lining by giving support to healthy intestinal mucosal cells, goblet cells, and to the immune system. Consider L-glutamine, essential fatty acids, zinc, pantothenic acid and vitamin C.

Why does the intake of probiotics sometimes produce bloating and gas in some people and not in others?

Not all people react the same to probiotics because it depends on their microbial populations. When a person has a poor diet (high simple sugars, low fiber), taking probiotics can produce gas. However, this usually goes away with time. If the patient increases complex carbs and decreases simple sugars that often decreases any gas and bloating brought on by the probiotic. When there are unexplained reactions to probiotics or prebiotics, it is a good idea to run an Organix test, a GI Effects test, or food antibody test to identify underlying imbalances.

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Part 1 can be read here

Great Plains laboratory and the other main dysbiosis testing labs in the USA

 Tuesday, March 3, 2009

In the USA, perhaps the 3 best known 'niche' labs for dysbiosis are the following:

Genova Diagnostics
Metametrix
Great Plains lab

In this post, we will look briefly at Great Plains laboratory. Of the 3 above, Genova and Metametrix seem closely associated with Functional Medicine, whereas it's unclear where Great Plains affiliation lies (it looks like a stand-alone company). The Great Plains founder, Dr William Shaw, was interested in gas chromatography-mass spectrometry, and noticed that some patients had high levels of metabolites that he associated with yeast. his lab associates 'tartaric acid' with gut candidiasis. The lab itself seems geared towards autism in particular (autistic people often have 'bowel' issues). An initial impression is that he could be regarded as a maverick 'conservative' physician. you can see his introductory video here.

His expertise seems to be from a gas chromatography-mass spectrometry background, and so his lab is very interested in metabolites. But they do do the full range that someone would expect from these type of investigative niche labs (immune tests, metabolite tests etc). His lab hold workshops and online conferences.

It's not known if there are any differences in the labs or if one or the other is more preferable. Perhaps at this point, the only real way of knowing would be for someone rich to do the same test in all 3 labs.

One good thing about Great Plains is that they seem to be allowing people to order the tests direct, rather than using the old 'physician knows best' principle (which in truth seems like a job-protection blocker rather than best for the patient). This is a first impression, when looking at the website to order the tests. Mymedlab.com. Metametrix also allow direct testing through 3rd parties such as directlabs.com

None of the above labs are likely aware of systemic body odor and particularly fecal body odor of course. Even amongst niche labs and functional medicine, the problem is still not recognised

Since yeast is often mentioned as a possible factor in fecal body odor on the body odor forums, it's interesting to read Dr Shaw's views on gut yeast infection. This article may be tailored towards autism in particular, but perhaps fecal odor sufferers have a similar problem in that for some reason their gut always has problems controlling the gut flora. In the article, Dr Shaw hypothesizes that some people perhaps for some reason do not have the normal checks and balances that stop the gut flora going bad, and external help may be needed for maintenance.

http://www.greatplainslaboratory.com/home/eng/yeast.asp

The 3 main groups of microbes that are mainly thought to cause gut dysbiosis are yeast (probably candida in particular), bacteria (both bad, or displaced or overgrowth) and parasites.

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related links

Dr Shaw 1995 medical paper on a gut yeast infection case

comparison of analytes tested in their dysbiosis organic acids tests
Genova: (note) this is their full organic acid test
Metametrix: dysbiosis test only
Great Plains: dysbiosis test only

 posted by blogcontributor2 on 3/03/2009

Originally published: https://www.meboblog.com/2009/03/great-plains-laboratory-and-other-main.html 

Sufferer's website of body odor theories: Bodyodor777.com

 

Sufferer's website of body odor theories : Bodyodor777.com

Everybody has body odor, some more than others. This website is for those who have strong, chronic body odor and are trying to find an end to this torture. I have compiled my research in this web to help as much as possible. There is no definite remedy for everybody, but the concrete information in this web will facilitate your search to find a cure.This website, bodyodor777.com seems to be run by a sufferer trying to make sense of the maze of body odor (which as anyone with the problem knows, for the vast majority of sufferers is far more complex than society thinks). They have gathered their own ideas as to possible theories. It presents an interesting general overview of internal and external causes of strong, chronic body odor. Of particular interest is the Internal Causes section that in addition to the ones normally come to mind related to metabolic disorders, hormones, mouth, nose, throat, and intestines, it also discusses sources such as the gallbladder, kidneys, allergies, liver, food intolerance, acidic body, anorexia nervosa, and more.

http://www.bodyodor777.com/index.html

at https://www.meboblog.com/2009/01/sufferers-website-of-body-odor-theories.html 

Your gut : a bag and 2 pipes

 

Saturday, January 3, 2009

your gut : a bag and 2 pipes

stomach : small bag on the upper left abdomen. preparation bag. 

small intestine : long thin coiled pipe designed for maximum absorption
colon : wide shorter looping (one loop) pipe. recycling plant. loads of bacteria

The digestion system seems likely to play a part in fecal body odor and other metabolic body odors (e.g. secondary trimethylaminuria), so it's probably important we understand it best as possible. This post is about the basic visual and mechanical structure and main purposes. What does the gut look like and do ?

Stomach : a small bag on the upper left hand abdomen. This is where food first ends up. Generally it is held here and turned to mush and then released into the small intestine through the pyloric valve in small controlled amounts. Simple carbs won't stay long, whereas a meal will take a while. Hydrochloric acid is added to it, and some other things to make it easier to digest. The mush is called 'chyme'. Each part of the intestine is separated by valves.

Small intestine : A long thin pipe that coils in an overlapping way. This is the main absorption point. It is designed for maximum absorption of molecules of a certain small size. There are millions of finger-like microvilli on the lining (like a carpet) to make 'catching' the molecules easier. It's this microvilli that is wiped out in full-blown celiac. The pancreas puts digestive enzymes into the pipe early on to break down the food, and bile is also squirted in by the gallbladder to digest fats. The absorbed molecules go into the portal vein and then are taken to the liver for filtering before entering the main circulation. The intestine acts as a barrier so that large molecules cannot get into the portal vein unless broken down. With leaky gut (which is really leaky small intestine), large molecules can get through junctions in the barrier and so are absorbed when they shouldn't be. Because you want maximum absorption here, there is usually very few gut microbes here, especially at the top end, largely because they would compete with you for the food. The small intestine is known as 3 parts ; duodenum, jejunum, ileum. Many feel that when someone has gut candidiasis overgrowth, it's growing at the ileum (for example). However, it's likely that overgrowth of anything in the colon will cause problems too. The small intestine and colon are separated by the ileocecal valve.

Large Intestine/colon : A short, wide pipe that ascends from your appendix area, goes up to your ribcage and across, and down the other side and then loops to the anus. the colon is where most bacteria is, even in a healthy gut. Good flora scavenges from any leftover food/chyme and many produce helpful fatty acids. The protein/sulfur eating bacteria tend to be at the lower left side of the colon (near the end). The chyme becomes feces as water is absorbed and the 'rubbish' is then exited.

It's probably more complicated than that but hopefully this gives you an image in your mind of what the gut mechanically looks like.

What goes wrong ?

Some examples. If anything is wrong with the digestion enzymes such as HCL, pancreatic enzymes, bile etc, you can end up with too much undigested food entering the colon which will likely alter the flora ecology detrimentally. for instance too much protein getting into the colon.

If the tight junctions in your small intestine barrier cells are weakened you can absorb molecules too big that are not intended to be absorbed. These enter the portal vein and are sent to the liver which likely regards these as unexpected molecules.

If conditions aren't right, perhaps microbes can colonize the lower small intestine or further up.

Perhaps the colon microbes can be unnaturally altered and produce toxins. In Secondary TMAU, the diagnosis means there is too much trimethylamine produced. It's currently thought the bacteria that produce this are in the colon, so it means overgrowth of this bacteria. Who knows if this bacteria can grow in the small intestine as well. Presumably no-one is currently looking whereas a Body Odor & Research center likely would be.

at https://www.meboblog.com/2009/01/your-gut-bag-and-2-pipes.html