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Showing posts from April, 2017

Homeless people, sweaty body odor and alcohol

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 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 enzyme and the related butyrate and propionate enzymes.

Diet, medicinal clay and large doses of a histamine-1 receptor blocker does reduce body odor in the bromhidrosis with elevated TSH type drastically

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 strong sweaty smell of 'apocrine' bromhidrosis seems caused by an enzyme defect in the propionate and butyrate degrading enzymes

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 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 enzyme. As a result it is very likely that a strong 'sweaty' s

The fecal body odor smell type

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

Trimethylamine (TMA) and the smell of fish

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