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Blog Archive

Tuesday, April 24, 2018

Danny Kunz: Secondary TMAU, TMA, & fish smell

The research in the last decade assumed a kind of wrong type of bacteria in the gut, which would produce large amounts of TMA just by introducing them into the intestinal tract. This assumption seems to be incorrect.
Since TMAU was discovered in the 1990s, it was assumed that there was a bacterial overgrowth in the gut that produced excess amount of the odorous chemical compound, trimethylamine (TMA), and thus, overwhelmed a deficient FMO3 metabolic enzyme in the case of Primary TMAU, or even overwhelmed a well-functioning FMO3 metabolic enzyme, in the case of Secondary TMAU. It was well understood by these scientists that this was only an assumption, since research funding had not been provided to identify which bacteria inhabited the human gut that would produce excess TMA. For this reason, a course of antibiotic treatment is recommended in the well-referenced TMAU odor-management protocol.

Historically, all research investment into TMA producing bacteria had been made in the fishing industry to determine the freshness of the fish, since it's more lucrative than investing in human research whose lives are devastated with TMAU.
In 2017, as a result of the gut microbiome studies the MEBO community has donated to both Danny Kunz and his Citizen Research Group in Germany and MEBO's Scientific Director, Irene Gabashvili, PhD., the data collected suggests that the elevated levels of TMA is not due to a bacterial overgrowth.  Irene's perspective will be posted at a later date in this blog.

Danny Kunz's observations suggest, "It is very likely that a permanent malabsorption of choline and betaine is the cause of the altered bacterial metabolism activity."


Trimethylamine (TMA) and the smell of fish
April 11, 2017

It is very likely that a permanent malabsorption of choline and betaine is the cause of the altered bacterial metabolism activity.
The typical smell of (dead) fish is based on a chemical compound called trimethylamine (TMA)...

The second type [of TMAU] is different. Patients with the type 2 pattern show an overload of the FMO3 enzyme caused by a largely increased TMA synthesis in the small intestinal tract.

The research in the last decade assumed a kind of wrong type of bacteria in the gut, which would produce large amounts of TMA just by introducing them into the intestinal tract.

This assumption seems to be incorrect.

Today’s view shifts currently. It is very likely that a permanent malabsorption of choline and betaine is the cause of the altered bacterial metabolism activity.
More interestingly most of the TMAU sufferers do have other dominant smell types than fishy. The most stated type of smell was a fecal smell.

In March 2009, MEBO interviewed Nigel Manning, Principal Clinical Scientist, Dept. Clinical Chemistry, Sheffield Children's Hospital, explained to us that more research had been carried out and papers published on trimethylamine (chemical with dead fish odor) and 'fish-spoiling' than on TMA in humans. Historically, all research investment into TMA producing bacteria had been made in the fishing industry to determine the freshness of the fish, since it's more lucrative than investing in human research whose lives are devastated with TMAU. When asked what bacteria is responsible for the production of trimethylamine in the gut, he replies,

Do we know what bacteria is responsible for gut Trimethylamine (TMA) production ?

NM: There are more than 400 species of bacteria in the colon but only a few described as TMA-producing. The fishing industry’s research microbiologists have published many papers on TMA and ‘fish-spoiling’ and cite species such as Vibrio harveyi, Vibrio fischeri, Photobacterium leiognathi and Shewanella baltica. The last of these is also know to generate hydrogen sulphide – or ‘ rotten egg’ gas. Whether these microbes are those responsible for human TMA production is a good question, but they may represent a small portion of the total.

For a description of these microorganisms, see a post in this blog, "Shewanella baltica and other TMA producing bacteria in the gut".


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Danny Kunz on Fecal body odor smell type

Danny Kunz and the Citizen Research Group he is a member of, created a blog, BODY ODOR RESEARCH BLOG, in which they talk about different types of body odor, i.e., fish, fecal, sweaty body odor, and TMAU, Bromhidrosis, Candida pathogenesis in Bromhidrosis, IBS, tight junction, and many other topics.

In the MEBO Annual Conference, Savannah 2018, we discussed some of these topics, including the extensive Food diet lists for fecal body odor and Bromhidrosis patients.


The fecal body odor smell type

April 12, 2017

So for people being TMAU negative and having a fecal body odor type it is very likely to have an enzyme defect in the histidine degradation pathway over the HNMT enzyme.
As stated in an earlier post, the most prominent reported smell type for TMAU2 patients was the fecal smell type. But not only TMAU positive patients reported such a type of smell, another body odor sufferer type do show the same fecal body odor pattern. Interestingly nearly all of those non TMAU patients report having Irritable Bowel Syndrome (IBS) as well. We took a closer look into the combined bacterial and human metabolism. The central chemical compound involved in the fecal smell seems to be indole.

Indole is produced within the bacterial metabolism as a precursor of tryptophan. As major source the bacteria use glycolysis based on sugar, carbohydrates, ...


To let the bacteria produce too much indole we found certain criteria:
- Tryptophan absorption of the intestinal cells is lower than the serine and glycine absorption
- Histidine malabsorption is present
- Tyrosine malabsorption is present

Why do TMAU2 patients now show a fecal smell, don't they have a choline and betaine malabsorption?

Yes, they have, but it seems that there are several different enzyme defects in the choline degradation pathway leading to such a choline malabsorption.

Some of those defects do also have an indirect impact on the histidine degradation over the histamine n-methyltransferase (HNMT) enzyme, which leads to a histidine malabsorption also.

Additionally the tryptophan and tyrosine degradation is further cuppled to the histidine degradation and as a result they show a tryptophan and tyrosine malabsorption also.

So for people being TMAU negative and having a fecal body odor type it is very likely to have an enzyme defect in the histidine degradation pathway over the HNMT enzyme.



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Monday, April 23, 2018

Conference Presentation by Danny Kunz



As usual, Danny Kunz most graciously provided the MEBO community with a very informative PowerPoint presentation on the Causes of Body Odor. This PowerPoint was to be presented and discussed at length at the MEBO Annual Conference, Savannah, Georgia 2018. Since we did have some technical difficulties and we were unable to hear the video, I am now presenting it here.

Discussion below on some points of interest that Danny tells us:

Histamine in the gut is bad because it has a strong impact on tight junction regulation of intestinal cells. In fact, "fecal body odor seems to be related to histamine degradation deficiency" The significance of gut wall health (tight junction regulation of intestinal cells) was discussed in the conference. Sufferers are recommended to consult with their physician if they experience prolonged allergic reactions, especially of the bowels, such as food sensitivities and/or indigestion, etc.

It is important to maintain good health of the digestive tract in the fight against odor conditions and PATM. Sufferers are recommended to consult with their gastroenterologist when experiencing any intestinal discomfort, including but not limited to, bloating, constipation, diarrhea, abdominal tenderness, painful bowel movement, hemorrhoids, rectal bleeding, etc.


It looks like histamine concentrations are highly important for the tight junction regulation of intestinal cells.

The tight junctions are important for the direct paracellular transport of electrolytes into the blood without transition through the intestinal cell metabolism.

Increased open tight junctions [leaky gut] will further lead to an increased surface area of the intestinal cells [IBS] and are as a result, a strong regulator of passing amines and their level of being processed.
http://bodyodorresearch.blogspot.com/2017/05/histamine-has-strong-impact-on-tight.html


Clinical significance of the opening of intercellular tight junctions (increased intestinal permeability), any of which may result in opening of tight junction, resulting in the passing of electrolytes into the blood without transition through the intestinal cell metabolism.

Clinical significance [Wikipedia]


The opening of intercellular tight junctions (increased intestinal permeability) allows uncontrolled passage of substances into the bloodstream, with subsequent possible development of immune and/or inflammatory reactions.[3][8]
The opening of intercellular tight junctions (increased intestinal permeability) can allow passage of microbes, microbial products, and foreign antigens into the mucosa and the body proper. This can result in activation of the immune system and secretion of inflammatory mediators.[12]
Increased intestinal permeability is a factor in several diseases, such as Crohn's diseaseceliac disease,[13] type 1 diabetes,[14]type 2 diabetes,[13] rheumatoid arthritisspondyloarthropathies,[15] inflammatory bowel disease,[8][16] irritable bowel syndrome,[9]schizophrenia,[17][18] certain types of cancer,[8] obesity,[19] fatty liver,[20] atopy and allergic diseases,[14] among others. In the majority of cases, increased permeability develops prior to disease,[8] but the cause–effect relationship between increased intestinal permeability in most of these diseases is not clear.[16][21]

For a clearer understanding of the above used terms, see illustration below:
  1. Transcellular route (pathway): The route through cells, as opposed to between the cells.
  2. Paracellular route: the route between cells
  3. Tight junction: A type of cell junction formed between epithelial cells of vertebrates wherein the outer layers of two adjacent cells fuse, thereby serving as a barrier to the passage of fluid between cells
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María

María de la Torre
Founder and Executive Director

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