Body Odor Research Blog

Glutamine and its counterpart glutamate seems to increase the butyrate production in the intestinal tract. Butyrates show a biting or pungeant, light sweat like smell. This strengthens the view that the tight junction sealing is dominated by metabolite pathways that present in one or the other way highly smelling chemical compounds the body is forced to absorb to counter regulate its deregulated energy metabolism in the intestinal tract .

Metabolic flux alignments showed first indications that the ammonia production might be reduced in some bromhidrosis cases. This might leed to fast glutamine drainage in intestinal cells. As a result glutamine supplementation might help ameliorating the low levels of glutamine and the reduced antioxidative effects in the cells. A test with CACO2 test cells from the collegues from the alcoholism research showed promising results with glutamine as well. A further supportive candidate is quercetine which is an antioxidant and a propsed inhibitor of the protein kinase which is related to the cAMP signaling. The cAMP signaling might be overactive in the same bromhidrosis cases. The cAMP signaling is calcium and Vitamine D dependent, in the form that calcium and Vitamine D do further overactivate the cAMP signaling, which might have negative impacts.

Collegues from the research field of alcoholism had a first succes in lowering the negative tight junction effect of acetaldehyde which seems to be one of the major malregulation factors in Bromhidrosis with TSH+. They used NAC successfully  in CaCo-2 cell tests. NAC is widely available as Supplement.

Based on the data of the USDA Food Composition Database we extrapolated four groups of foods. The respective lists can be found here: https://drive.google.com/folderview?id=0B9gtX6As3TJGa25zX1ZvNmZROUU

Our observation was that bromhidrosis patients reported slight elevated candida sp. levels in combination mit reduced enterococcus sp. in stool analysis results. The current metabolism impact for bromhidrosis seems to be sourced in a deficient acetate or propionate degrading enzyme which is part of the major ethanol degradation. The biosynthesis of ethanol is mostly based on candida sp., so we investigated into the pathogenesis of candida. The following pictures show the resulting disease model. In the case of an deficiency in the ethanol degradation pathway, the immune system shows a weakness regarding the candida sp., which shifts the microbiome towards increased candida occurence and activity. This would lead to small intestinal fungal overgrowth (SIFO) symptoms 

Several TMAU2 positive tested people reported that their body odor symptoms increased strongly in stress related situations. As we now have included the noradrenaline and adrenaline degradation path, the metabolism map shows a high impact in both pathways. If a enzyme defect around the BHMT enzyme is assumed, the result would be that the intestinal tract runs very fast out of SAM (S-adenosyl-methionine). Low SAM levels would of course be further drained by the release of noradrenalin and adrenaline. In both degradation pathes the COMT enzyme is responsible for the further drain of SAM. RNA expression of the COMT shows clearly that COMT is not only present in the brain, instead in the intestinal tract, liver, etc. as well. The COMT enzyme was once the major target of schizophrenia research. Today it seems that the body odor diseases are strongly related to enzymes which cause schizophrenia and depression. The main difference is that those enzymes are in the body odor cases locally

Today we release a new curated metabolism map regarding body odor diseases. The new map alignes around the main inhibited enzymes by body odor diseases. Beside of that a first receptor linkage has been included. The map further shows now measured chemical compounds in unnormal ranges of tmau2 and bromhidrosis with elevated TSH. Obviously in the tmau2 case the measurements align pretty good with the assumption that the intestinal tract metabolism runs out of SAM (S-adenosyl-methionine) by defects in the homocysteine to methionine conversion. https://drive.google.com/file/d/0B9gtX6As3TJGTDVfNDRfek1WLTA/view?usp=drivesdk

A lot of people do misunderstand the impact that body odor diseases have. So how does a visual comparison look like?

In previous posts was mentioned that the fecal body odor seems to be related histamine degradation deficiency. What impact does that have? 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 will further lead to an increased surface area of the intestinal cells and are as a result a strong regulator of passing amines and their level of being processed. One of the regulation relevant receptor for the tight junctions is the H1 receptor. When mast cells e.g. get active they release histamine to open those tight junctions. So a relation to food allergies as a initial trigger seems to be a possible factor with an upfollowing malregulation of the histamine concentrations. The malregulation would be based on the increased histamine level

Everyone once in their lifetime encountered a homeless person which presented itself with a strong sweat like smell. Most people do relate this to poor hygiene, even if that smelly person does not show outer signs of poor hygiene. For some homeless people poor hygiene might be a reason, nevertheless from a metabolic point of view there might be an alternative major reason: higher alcohol consumption in combination with lower food intake If we look at the ethanol degrading pathway, we realize that it compromises the EC 6.2.1.1 in an overload situation pretty similar to the case when people having a primary enzyme deficiency in this enzyme. As a result it might be that the Clochard Smell Syndrom is caused by an metabolic impact on the EC 6.2.1.1 enzyme and the related butyrate and propionate enzymes.

In an explorative case with strong sweaty body odor, normally associated with 'apocrine' bromhidrosis, the odor emission reduces drastically after two weeks of large doses of loratadin (>50mg daily) During that period a diet was in place: - exlusion of high histidine foods - exclusion of sugar holding foods - meals did contain only proteins or carbohydrates but no mixture of both During that period following supplements were taken: - DAO - Vitamine C (1000mg) - Medicinal clay especially for histamine intolerance

The classical view of dermatology regarding the cause of a strong sweaty underarm odor is that a defect function of apocrine sweat glands is present. As a result dermatologists consider chirurgical removal of the apocrine sweat glands as the only way to treat such an odor. We made a chemical analysis of clothes of patients using GC-MS. On the outer limit of the GC was a peak in butyric acid shown. Butyric acid seem to build up in the clothes of patients over time. When we investigated into the human metabolism regarding butyric acid we found immediately the butyrate degrading enzyme  EC 6.2.1.2 This enzyme is mostly present in the liver, degrading butyrates (butyric acid salts) which are taken up as main energy source for the large intestinal tract sourced by the bacterial fermentation processes within the gut. The same pattern applies to propionates (propionic acid salts) which are degradated by the EC 6.2.1.17 enzyme. As a result it is very likely that a strong 'sweaty' s

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 Syndrom (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

The typical smell of (dead) fish is based on a chemical compound called trimethylamine (TMA). Fish do use it in the regulation of their metabolism during pressure changes. For humans there is a body odor disease known as trimethylaminuria (TMAU) This desease has two types.  The first type is based in a defect of the FMO3 enzyme found in the human liver metabolism and people affected by that do emit a fishy odor. The second type 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.  Todays 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