Systemic body odor and/or halitosis sufferers in Ireland can be referred to Dr Eileen Treacy in Dublin

Finding expert help for systemic body odor and/or halitosis can be very difficult if not impossible (for most it is impossible). However, sufferers in Ireland who feel their odor problem is systemic can be referred to Dr Eileen Treacy at the National Centre for Inherited Metabolic Disorders in the Childrens University Hospital in Dublin. Dr Treacy gave us permission to publish her instructions for referral in a post. The person must go through their Irish GP to get an appointment. Dr Treacy wrote :

We are happy to take Irish referrals. These should be made by writing (not email) from the individuals’ GP to the address below (National Centre for Inherited Metabolic Disorders).

Best wishes,
Eileen Treacy

Prof. Eileen Treacy,
Metabolic Consultant,
National Centre for Inherited Metabolic Disorders
Childrens University Hospital,
Temple St.,
Dublin 1

Dr Treacy has a respected history in TMAU research, with pubmed papers dating back to 1998. She worked as a pediatrician at the McGill University Hospital in Montreal, and possibly was an influence as to this hospital being one of only perhaps 3 labs who test for TMAU genotype (the urine test) in North America.

Dr Treacy has mentioned before that TMAU may warrant being added to newborn screening tests, and that the estimate for 'severe' TMAU (the classic type, where the person has 2 mutant copies) may be not greater than 1/5000 (which would be 60,000 in the USA), but that it is not known how many may have the milder types.

Her involvement in TMAU papers can be seen in this link
Pubmed papers about trimethylaminuria involving Dr Eileen Treacy

Some notes about papers Dr Treacy has been involved in :

2000 paper : typically TMAU is taught as being 2 mutant copies, but this paper mentions that polymorphisms, that are usually much less severely affected copies, in the case of FMO3 function may be an issue.

The results imply that prevalent polymorphisms of the human FMO3 gene may contribute to low penetrance predispositions to diseases associated with adverse environmental exposures to heteroatom-containing chemicals, drugs, and endogenous amines.
http://dmd.aspetjournals.org/cgi/content/full/28/2/169

2002 paper: In vivo variability of TMA oxidation is partially mediated by polymorphisms of the FMO3 gene

...We have previously described a number of FMO3 polymorphisms which in vitro exhibit reduced substrate affinity for several FMO substrates. Here we show that three prevalent polymorphisms (E158K, V257M, and E308G) inherited in particular combinations confer a slight decrease in TMA oxidation under normal physiological conditions, which may be clinically "silent." With the use of substrate loading or with the interaction of other known modulators of FMO3 activity such as hormonal influences, these genotypes may predispose to mild TMAU

http://www.ncbi.nlm.nih.gov/pubmed/11461189

2005 paper : Polymorphisms of the Flavin containing monooxygenase 3 (FMO3) gene do not predispose to essential hypertension in Caucasians
In this study conducted in Ireland, a large sample of high blood pressure and hypertension sufferers were compared against a group of healthy people with common FMO3 polymorphisms, with the hypothesis that such FMO3 polymorphisms could potentially predispose the person to high blood pressure and hypertension. Tyramine is a good FMO3 substrate and known to be involved with blood pressure control. The study found no link.

CONCLUSION: These results suggest that the variants in the FMO3 gene do not predispose to essential hypertension in this population.

http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=16324215

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Related links :
1998: Mutations of the flavin-containing monooxygenase gene (FMO3) cause trimethylaminuria, a defect in detoxication

OMMBID chapter on trimethlyaminuria written by Dr Eileen Treacy. The abstract is free but the full chapter costs around $30(?)