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Showing posts from June, 2017

Candida pathogenesis in Bromhidrosis

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 

TMAU2 and the 'schizophrenia' of the intestinal tract

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

Body odor metabolism map (V20)

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.