Findings found that the use of “fecal/sewage” as a description, and the use of multiple descriptors of the smell, and incorrect locations of smell origin effectively differentiated ORS from TMAU. In the literature on body odour identification, emphasis is frequently placed on multiple consultations to reduce the risk of misdiagnosis, and also asking the individual to have a reliable confidant accompany them to the consultation who can confirm the reality of the reported symptom. ORS patients are unable to provide such confidants as they have no objective odor.A fecal smell (fecal body odour) is often a self reported symptom associated with TMAU, however there is no recorded evidence of fecal body odour present in any study related to TMAU. Cashman JR found that 53% of TMAU and 59% of non-TMAU subjects suffered from regular halitosis, dental plaque on the back of the tongue, which produced on average "200-600 ppb of sulfurous/fecal smelling volatile sulfur compounds (i.e., VSC: hydrogen sulfide; methylmercaptan; dimethylsulfide) with each exhalation, creating a “malodorous cloud” in their vicinity. It is likely that halitosis, ORS or in severe cases, a bowel obstruction leading to fecal vomiting may be the cause. There is the possibility that someone may suffer from both Trimethylaminuria and ORS-like paranoia, due to the potential lack of ability to smell the odour oneself and the worry that it generates. It is recommended to organise reliable confidants, colleagues, friends or relatives ("smell buddies") to work with the sufferer to discretely inform them if they are presenting an odour.
Trimethylaminuria (TMAU), also known as fish odor syndrome or fish malodor syndrome, is a rare metabolic disorder that causes a defect in the normal production of an enzyme named flavin-containing monooxygenase 3 (FMO3). When FMO3 is not working correctly or if not enough enzyme is produced, the body loses the ability to properly convert trimethylamine (TMA) from precursor compounds in food digestion into trimethylamine oxide (TMAO), through a process called N-oxidation. Trimethylamine then builds up and is released in the persons sweat, urine, and breath, giving off a strong fishy odor or strong body odor. Primary trimethylaminuria is caused by genetic mutations that affect the FMO3 function of the liver. A variant of TMAU (secondary trimethylaminuria or TMAU2) is an acquired form of TMAU where there is no genetic cause, yet excessive TMA is secreted. TMAU2 can be caused by a range of issues, including a precursor overload (ingesting too many precursors), hormonal issues related to menstrual cycles, liver damage, and liver and kidney failure. It is hypothesised that intestinal dysbiosis may cause temporary TMAU2 symptoms, however there is no direct evidence of this in a scientific study. Metabolic pathway
Trimethylamine enters the body via the consumption of certain foods and supplements. When food is consumed that contains TMA and/or TMAO (predominately seafood; saltwater fish, shellfish, seaweed and kelp), TMAO is converted by bacteria in the lower gastrointestinal tract (gut) into TMA.