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anti-TMA pill in a year or 2 ? (scroll 12 mins)

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MEBO TMAU TESTING DISCONTINUED
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MEBO Map Testing & Meetups


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MEBO - UBIOME study 2018

'PRESS RELEASE'

NCT03582826
ClinicalTrials.gov

MEBO Gut Microbiome Study
"Microbial Basis of Systemic Malodor and PATM Conditions (PATM)"
Funded by uBiome Research Grant

"Microbial Basis of Systemic Malodor and PATM Conditions (PATM)"

Dynamics of the Gut Microbiota in
Idiopathic Malodor Production
& PATM

Started May 2018 - Ongoing

Current people sent kits : 100/100
3 kits per person

NO LONGER RECRUITING

Participation info : LINK English

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TMAU Petition world
TMAU UK end total:262
TMAU UK ends 23/01/20
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USA : Moveon open
TMAU (Dominican)
Metabolomic Profiling Study
NCT02683876

Start : Aug 2016
Stage 1 : 27 Canadian volunteers to test
Latest click here (26 oct) :
17 samples returned


Note : Stage 1 is Canada only.
Return cut-off date : passed
Analysis can take 6/8 weeks
Analysis start in/before Nov
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Denver TMAU Test Lab survey click here
click to Read more/less

USA survey for anyone who wants to improve Denver TMAU test

begun : Dec22
end : no ending for now

A trainee genetic counselor is working at the Denver TMAU test lab. Probably as part of her training. As a project she wishes feedback on any aspect of the Denver TMAU test and process. You can fill in the survey and/or email her (email address is in survey). It's meant for USA people, but perhaps others can give their view too (as we have so few opportunities).

quote from her rareconnect post

"Hello all! I wanted to make you aware of a research study being conducted to better understand the experience and needs of individuals with trimethylaminuria with a goal of being able to create improved patient and healthcare provider education materials. Any participation is completely voluntary and all responses remain confidential. Feel free to use the contact information within the link with any questions or share the survey with others with TMAU."

see this post for more details

https://www.meboblog.com/2023/01/denver-tmau-test-survey-tbc-who-it-is.html
Showing posts with label interview with experts. Show all posts
Showing posts with label interview with experts. Show all posts

Friday, November 15, 2013

Spanish TMAU forum moderated by a Dr with an interest in metabolic disorders

Dr Mercedes Serrano is a child neurologist at Hospital San Joan de Deu, Barcelona who understands the importance of the internet as a means of communication about rare disorders. She moderates the website www.guiametabolica.org which is in Spanish but there is a google translate button on each page so that you can get a decent translation in most languages. So far the Trimethylaminuria forum has 89 members and Dr Serrano answers questions personally when she can. She recently gave a webinar in Spanish about TMAU in the rareconnect.org webinar platform but this does not appear to be archived (yet).

Here is the guiametabolica.org TMAU forum
Here is the guiametabolica.org TMAU home page
Use the google translate button at the top of the pages for a decent translation

Below is a video Dr Serrano did for rareconnect.org about the guiametabolica website

Monday, September 16, 2013

Prof Elizabeth Shephard's Radio Show Interview


Pythagoras’ Trousers, The Science & Technology Radio Show
Episode #131, [time frame 0:41 – 12:20]
Program: Fish Odor Syndrome
September 12, 2013
Rhys Phillips

Elizabeth Shephard, PhD
Professor of Molecular Biology
Vice Dean Education, Biosciences
Institute of Structural and Molecular Biology
Division of Biosciences
Darwin Building, UCL Genetics Institute
University College London
MEBO Research Scientific Advisor
Member of the MEBO Institutional Review Board

University College London
Gower Street
London, WC1E 6BT



It [Primary TMAU] is a genetic disorder caused by a bad gene and not because people have bad hygiene.
Professor Elizabeth Shephard, MEBO's Scientific Advisor and Member of the MEBO Institutional Review Board is interviewed by Beth Berry on TMAU, and describes the physical and psychological manifestation of TMAU, and explains the different genetic both Primary and Secondary form of TMAU.

[2:09] “It [Primary TMAU] is a genetic disorder caused by a bad gene and not because people have bad hygiene.”

She also explains the genetics of Primary TMAU. The most affected individuals’ defective genes are passed down from both mother and father [3:31] in the case of homozygous (receive two bad copies of the gene - one from each parent). The milder form heterozygous for the condition inherits one good gene from one parent and one bad gene from the other parent [3:49], but would produce enough protein that the patient would not necessarily have the condition of TMAU.

[4:00] Dr. Shephard also explains the genetics of the Transient Form of TMAU that affects children.

Episode #131, [time frame 0:41 – 12:20]
Program: Fish Odor Syndrome

Click on the following link to listen to the Radio Show Interview

http://www.rhysphillips.co.uk/pythagoras-trousers/episode-131/



mebo trinzyme project


[8:15]Beth Berry: Dr. Shephard tells me that there are research teams currently looking at these viable compounds to be used as therapeutic drugs, but it is not a quick or simple process to produce a treatment, as she explains.

HOW TO RESEARCH A THERAPEUTIC:

Professor Shephard: For any therapeutic, first of all, scientists have to discover a therapeutic, and then has to go through a series called Pre-Clinical Tests to understand the use of that therapeutic; does it do its job properly, make sure that it’s not toxic, and that it could potentially deliver when administered to patients? Then it has to go through a whole series of legislation to make sure that it will be safe. And then, when we talk about Clinical Trials, the therapeutic will be tested in healthy individuals to understand what the therapeutic does and to make sure there are no adverse effects. Only at that point would the therapeutic be permitted to be used for the treatment of individuals with a particular disorder. [9:14]

INTERNATIONAL SUPPORT NETWORK:
[9:15]Beth Berry: This condition is far from easy to live with, and so a support network is incredibly useful to people who suffer from this condition and who find it particularly detrimental. Support networks and websites have been set up where people can find advice on how to manage symptoms or how to explain their condition to friends, family, or co-workers. [9:38] These organizations also aim to spread information about this condition far and wide. As once we become more understanding of this condition, it is also likely that we will become more tolerant of it, and thus ease the suffering experience by patients. [9:52]


there are a number of different mutations, but they all influence the same protein
[9:53] Professor Shephard: We now have the internet, so it is easier to find information on the disorder, easier to take information to a medical doctor should you suspect you have this disorder, in case the medical doctor has not heard about the disorder.
[10:10] If a person does think that they have TMAU, the best thing to do is to consult a medical doctor, and to ask if a urine test could be carried out. A genetic test is something that would really come later and only if the person decides it. So the disorder can be detected by the urine analysis; the genetic test will confirm the mutation that the particular family might carry or that particular person might carry. [10:34] So, there are a number of different mutations, but they all influence the same protein, they just make different changes, some are more severe than others.


TMAU URINE TEST:
So, by understanding how much TMA there is relative to TMAO gives an indication of how well the enzyme is working.
Professor Shephard: [10:49] The urine test for TMAU tests for the amount of Trimethylamine (TMA) in the urine and it tests for the amount of Trimethylamine N-Oxide (TMAO). [11:00] The TMAO is the chemical that is produced by FMO3. TMAO is the chemical that does not smell and TMA is the chemical that does smell.

[11:07] So, by understanding how much TMA there is relative to TMAO gives an indication of how well the enzyme is working. So the less TMAO would indicate that the enzyme is not doing its job very well, and the more TMAO present, then the enzyme is doing its job better. [11:33]A person can be severely affected and might excrete 90% TMA and only 10% TMAO. Or a less severe person might excrete about 50% TMA and 50% TMAO. And that is really dependent on the individual, and the change in their gene that has affected their particular protein, and its ability to do its job. [12:01]

[12:02] I think we’ve reached the stage of scientific discover where it is now possible to think about the best ways of providing therapy for the patients. [12:14] Different groups will explore different therapeutic possibilities, but we all have the common goal to find a therapy that will help the patients to overcome the symptoms of Trimethylaminuria. [12:24]
See Orphanet link to research project

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María de la Torre
Founder and Executive Director

A Public Charity
www.meboresearch.org
www.brasil.meboresearch.org
maria.delatorre@meboresearch.org
MEBO's Blog (English)
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Saturday, March 30, 2013

Digestive System and Body Odor / Halitosis


Throughout human history, there are seemingly countless remedies and treatments passed down from generation to generation. A very long list of articles have been written by experts from different fields of health approaches on digestive health, but very few, if any, give serious attention and discussion exactly how the digestive system affect body odor and halitosis. On May 11, 2009, MEBO Research posted in this blog an interview conducted with Cass Nelson-Dooley, Clinical Consultant at Metametrix, with contributions by Mr. Tony Hoffman.

In Part 1 and Part 2 of the interview, questions were asked with the sole purpose of trying to determine what it is about our digestive system that could be causing, or at the very least contributing to the various types of body odor and halitosis. The readers of this blog are encouraged to read these posts and to write comments below on any additional scientific/medical source that further discusses involving the opinion of professionals.

Many sufferers describe their odor to be fecal, so we asked Cass Nelson-Dooley about that. She replies,


The smell of feces comes from short chain fatty acids (SCFAs) and bacteria like E. coli. All the SCFAs have strong smells. Butyric acid is an SCFA and it smells like feces and even like body odor. E .coli has more of a mousy odor.

Cass also gives her opinion about the use of probiotics and prebiotics.

Not all people react the same to probiotics because it depends on their microbial populations. When a person has a poor diet (high simple sugars, low fiber), taking probiotics can produce gas. However, this usually goes away with time. If the patient increases complex carbs and decreases simple sugars that often decreases any gas and bloating brought on by the probiotic. When there are unexplained reactions to probiotics or prebiotics, it is a good idea to run an Organix test, a GI Effects test, or food antibody test to identify underlying imbalances.
When asked if there is a general treatment advice, she refers to the
“4R Protocol.”

I think the “4R Protocol” is the most general treatment advice and it’s comprehensive, but every doctor has a different approach and dysbiosis treatment should be tailored to the patient…
Remove offending foods, medications, gluten (if sensitive) and reduce poor quality fats, refined carbohydrates, sugars, and fermented foods (if yeast is present). Consider antimicrobial, antifungal, and/or antiparasitic therapies in the case of opportunistic/pathogenic bacterial, yeast, and/or parasite overgrowth (see below for specific recommendations).
Replace what is needed for normal digestion and absorption such as betaine HCl, pancreatic enzymes, herbs that aid in digestion such as deglycyrrhizinated licorice and marshmallow root, dietary fiber, and water.
Reinoculate with favorable microbes (probiotics such as Lactobacillus sp., Bifidobacter sp., and Saccharomyces boulardii). To enhance the growth of the favorable bacteria, supplement with prebiotics such as inulin, xylooligosaccharides, larch arabinogalactans, beta glucan, and fiber.
Repair mucosal lining by giving support to healthy intestinal mucosal cells, goblet cells, and to the immune system. Consider L-glutamine, essential fatty acids, zinc, pantothenic acid and vitamin C.

Final question: Is stool DNA testing likely to be as good as stool microbial testing will get?

I think DNA analysis in stool testing is an enormous leap forward in technology. In the Manual of Clinical Microbiology they state, “PCR is the best developed and most widely used nucleic acid amplification strategy…These techniques have sensitivity unparalleled in laboratory medicine, have created new opportunities for the clinical laboratory to have an effect on patient care and have become the new ‘gold standards’ for laboratory diagnosis of several infectious diseases.” With DNA analysis, we are seeing the microbial population with more sensitivity and specificity than ever before. Doctors and scientists trained on the older culture techniques have to view DNA results with a fresh perspective. I think that stool microbial testing will continue to evolve and improve in ways that we can scarcely imagine today.


María

María de la Torre
Founder and Executive Director

A Public Charity
www.meboresearch.org
www.brasil.meboresearch.org
maria.delatorre@meboresearch.org
MEBO's Blog (English)
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Monday, September 24, 2012

TMAU/FMO3 webinar recording : Professors Shephard and Phillips

2ND Webinar on FMO3



This is the recording of the TMAU/FMO3 webinar that took place 23rd September 2012
Guest Speakers : Professor Elizabeth Shephard and Professor Ian Phillips
Webinar title : "FMO3 : bugs, genes and drugs"

The webinar was kindly hosted by Rob Pleticha of rareconnect.org
You can see the original post on rareconnect.org here : TMAU webinar
rareconnect.org has a TMAU community : rareconnect.org TMAU community

This is the first in a series of webinars with TMAU/FMO3 experts as guest speakers. There was also a previous webinar where TMAU sufferer, MEBO UK Director of Public Relations, Karen gave a talk on how to use the media to advance the Cause of people living with malodour disorders: Karen's TMAU talk.

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Wednesday, August 8, 2012

Antibiotics and obesity, illness, tendency for auto-immune diseases



MEBO Research UK's Community Director, Stephanie, brings to our attention this article, which is so very pertinent to our community because the TMAU Odor-Management protocol recommends the use of antibiotics to control TMAU symptoms, and possibly other types of malodor conditions, even though this has not been researched fully to the satisfaction of our experts. It is, however, the method that has given positive results in regards to decreasing malodor. Nonetheless, treatment with antibiotics needs to be researched further to identify the microorganisms producing odorous compounds and the best treatment to create an optimal gut flora. The TMA-producing bacteria in our gut has yet to be identified, as our experts tell us in their interviews for this blog. Lack of research funding for this much needed research only accentuates the need for proactive work in our Raising Awareness Campaign because it was only a few weeks ago that the research grant was denied.

A team of UK specialists who got together to write a grant proposal to the Medical Research Council (MRC) for research funding into the specific intestinal bacteria found in the trimethylamine odor suffered by TMAU patients. This research would have also explored the possibility of fecal bacteriotherapy/human probioticn infusion as a treatment for odor disorders, such as TMAU. Unfortunately, this grant application was turned down. Thus, we as sufferers from around the world have been deprived of a treatment possibility by the rejection of this application.


INTERVIEW WITH NIGEL MANNING
Q: Do we know what bacteria is responsible for gut Trimethylamine (TMA) production ?

A: There are more than 400 species of bacteria in the colon but only a few described as TMA-producing. The fishing industry’s research microbiologists have published many papers on TMA and ‘fish-spoiling’ and cite species such as Vibrio harveyi, Vibrio fischeri, Photobacterium leiognathi and Shewanella baltica. The last of these is also know to generate hydrogen sulphide – or ‘ rotten egg’ gas. Whether these microbes are those responsible for human TMA production is a good question, but they may represent a small portion of the total.

Q: Is the bacteria in the colon or small intestine ?

A: The distal part of the colon is responsible for protein and amino acid breakdown and I suspect the area for TMA production. Although there are hundreds of intestinal bacterial species there may be just 30 or 40 species which represent more than 90% of the microbes in number. If a TMA-producing species becomes predominant, eradication with antibiotics may prove to be very difficult. Apparently there are ten times as many bacterial cells in the human gut as cells making up the entire human body – making the gut flora a powerful metabolic force. Attempts at eradication with antibiotics such as metronidazole have been successful for TMAU2 sufferers – leaving them odour-free after a single course in some instances (as I mentioned earlier). Other antibiotics include neomycin and amoxicillin. Without specific identification of bacterial species involved (and their severity of overgrowth) the choice of an effective antibiotic for TMAU2 is often a question of trial and error. TMAU1 sufferers can also benefit from periodic antibiotic therapy as well as dietary choline restriction. Both TMAU1 and 2 can be controlled in similar ways, although the secondary (acquired) form has the possibility of a complete cure. TMAU1 may be controlled to some degree by antibiotics, restriction of choline (eggs, liver, beans) carnitine (meat) and TMA-oxide (seafood). The odour effects of TMA may also be reduced by activated charcoal or copper chlorophyllin tablets to adsorb TMA in the gut and the use of pH5 skin creams to neutralize TMA in sweat.


INTERVIEW WITH CASS NELSON-DOOLEY OF METAMETRIX
Q: Do you think a particular type of bacteria are responsible for gut trimethylamine production? Do you have a good idea what microbes in particular cause gas smells? Do you have any theories as to how someone could smell of gut smells through their pores/breath?

A: The more smelly compounds like trimethylamine and hydrogen sulfide are not products of human metabolism, but they are produced by several bacteria under certain conditions. They tend to be strict anaerobes that could dwell in the colon or the vagina.

It is likely that bacterial overgrowth occurs in the small bowel and the products are absorbed and then emanate from the skin. I wouldn’t expect that the malodorous products would be absorbed from the colon. If someone has an overgrowth of Disulfovibrio, there may be a sulfur smell. If someone has an overgrowth of Pseudomonas sp., the smell may be sweeter (grape-like), but still sickly sweet. There is a whole group of sulfur-producing bacteria. Citrobacter freundii produces sulfur. Additionally, if the person suffers with maldigestion then food will undergo fermentation and this produces putrefactive compounds such as putrescine. While blood borne body odor is likely multi-factorial, at least for some patients, healing the bowel and cleaning up the diet could provide some relief.



Instead of the repeated use of antibiotics, this Health online article focuses on diet to control bacterial populations in our gut. Dr. Zhao Liping, Microbiologist, recommends,


Keep these bacteria in the right balance and they can control weight, cut the risk of eczema in babies and keep old people stronger, it seems.
It may even be possible to use beneficial bacteria to switch certain genes on or off.
If all this is true, it could be another very good reason for avoiding antibiotics.



Read more: http://www.dailymail.co.uk/health/article-2184626/Antibiotics-How-taking-make-fat-ill-prone-auto-immune-diseases.html#ixzz22vAWYV2y

María

María de la Torre
Founder and Executive Director

A Public Charity
www.meboresearch.org
www.brasil.meboresearch.org
maria.delatorre@meboresearch.org
MEBO's Blog (English)
El Blog de MEBO (español)
MEBO Brasil - Blog (Portuguese)



SUPPORT THE MEBO MISSION: Click Amazon button at right sidebar of this blog when shopping online for the holidays
at no extra cost to you.
MEBO gets small commission from Amazon.


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Saturday, April 9, 2011

Professor Elizabeth Shephard TMAU/FMO3 slideshow for the MEBO Washington DC Conference 2011



This is a slideshow overview of TMAU in relation to the genetic deficiciency of FMO3 enzyme, kindly provided for the 2011 Washington DC Meetup by Elizabeth Shephard (Professor of Molecular Biology)
Vice Dean Education, Faculty Life Sciences, University College London, UK, who has a long history in TMAU/FMO3 research. Along with Prof. Ian Phillips, she authored the NIH gene reviews article on trimethylaminuria


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Monday, December 6, 2010

Interview : Dr John Cashman of HBRI in San Diego


helpful links :
CYP
CYP 3A4
DME's
FMO
FMO3
With the interviewee's permission, we have managed to compile a question and answer interview from a recent email dialogue about the enzyme Flavin containing monooxygenase isoform 3 (FMO3) with one of the leading experts in this group of enzymes (as well as expertise in many other human enzymes), Dr John Cashman of the Human Biomolecular Research Institute in San Diego. The dialogue was to try and understand more about FMO3 since sub-normal FMO3 is responsible for genetic trimethylaminuria. Dr Cashman has a long history in TMAU/FMO3 research, especially in the genetic field.
Dr John Cashman medical papers on TMAU/FMO3

We thank Dr Cashman for being so helpful to the TMAU community, and for his long association in research that is directly related to genetic TMAU.



Is FMO3 one of the most widely used enzymes we have ?
Based on the publications in the literature, I think FMO is underrecognized. It is present in adult liver to a great extent, almost 60% of the amount for the major CYP enzyme (CYP3A4) that does most human drug metabolism currently listed in the literature.

Is there a rule of thumb that we can use to know when something in the diet is likely an FMO3 substrate ? (eg. greenfoods, foods with sulfides, etc) It sounds like almost all vegetables, herbs, spices and proteins potentially.
Yes, FMO prefers smaller nucleophilic compounds: Sulfur-, Nitrogen-, Selenium-, and Phosphorous-containing compounds. But not all that contain these heteratom-containing compounds are nucleophilic as the atoms can be in aromatic rings and non-nucleophilic.

Are all (or many) sulfides, amines, and phosphates FMO3 substrates ?
These substrates need to be nucleophilic. Not all sulfides etc are nucleophilic. Phosphines not phosphates, and organo selenium compounds. But the enzyme substrate binding region has some size requirements or limitations.

Do you expect people with FMO3 deficiency could have problems with FMO3 substrates other than TMA ? (including endogenous)
Yes, I think there could be adverse drug reactions as the amines are not N-oxygenated, for example and are not rapidly cleared. There are many drugs that are amines but not enough research has gone into determining if any of these amine drugs are substrates for FMO. My suspicion is that many more than are currently recognized are substrates for FMO.

Is FMO3 the only likely Drug Metabolizing Enzyme (DME) associated with smells ?
I am not sure about this because other DMEs including CYP metabolize amines, sulfides and phosphines.

Can we survive with zero FMO3 function with no obvious problems apart from TMAU?
I am not sure that the experiment has been done in terms of making a FMO3 knock out mouse and looking at the consequences of this. My suspicion is that FMO3 is involved in some important mammalian developmental function that we don't recognize currently.


CYP3A4 seems to be inhibited by a wide range of chemicals which I presume may be constantly updated. We know that indoles inhibit FMO3. Do you think it is likely that more FMO3 inhibitors that are common in the diet are likely to be discovered?
FMO evolved to metabolize plant-derived materials. This was important early on as evolving mammals needed to protect themselves from all the nucleophilic materials in plants. Yes, I suspect there are a few more nucleophiles that avoided this process but I think most are detoxicated (N-oxides and S-oxides are metabolites). The problem may come in as reductases also evolved to retro reduce N-oxides and S-oxides. These may be more efficient and be the source of the problem. Another important issue is that sometimes FMO produces a reactive metabolite that does not inhibit FMO but leaves the FMO enzyme and inhibits CYP.

Endogenous compounds are compounds created in the systemic circulation. Are there any endogenous compounds that are good FMO substrates ? e.g. hormones or neurotransmitters or blood pressure regulators.
We have published that tyramine and phenylethylamine are FMO substrates. We looked at the other major ones and they do not appear to be substrates: Serotonin, Dopamine, Norepinephrine, Histidine apparently are not substrates for FMO3.

Is FMO present in the gut ?
Yes, FMO is in the gut. I think FMO1 and FMO5 more so than FMO3 but this is in a review with Jun Zhang we published years ago.
see: http://www.ncbi.nlm.nih.gov/pubmed/16402899

Looking at the list of inhibitors for CYP 3A4 on wikipedia (eg citrus, echinacea, milk thistle), It looks as if flavonoids are a particular problem for CYP enzymes? I wonder if these compounds could inhibit FMO3 ?
Probably not. But not sure on this one. Most of the CYP (inhibitors ?) in citrus are polycyclic flavonoids. No nucleophilic atoms are present. So it is unlikely non-nucleophiles are inhibitors. There is a report out there that caffeine is a substrate for FMO3. This is wrong. Not an inhibitor either. No nucleophilic centers. There are a number of azoles (ketoconazole) and imidazoles (cimetidine) that inhibit/alternate substrates for FMO3 but these are from nucleophilic groups in the molecule.

It has been hypothesized that if someone has a bad reaction to a drug it is more likely due to a DME enzyme deficiency rather than an allergy. What are your thoughts on this ?
I am not sure of this one. I think most reported adverse drug-drug interactions (DDIs) occur when there is an excess of a drug compared to normal clearance and reasonable therapeutic levels. There is a DOSE-dependence. Often with allergic reactions, dose is not that important and small concentrations can illicit an immune response. Most DDIs reported are related to liver metabolism.

Pepper is a spice that has anecdotally caused bad reactions such as nightmares.
Pepper inhibits gut metabolism and permits things to be more efficiently taken up through the gut. I dont believe this has been examined as a substrate or inhibitor of FMO.

Could there be an FMO connection with intolerance of garlic ?
Lots of people don’t do very well with garlic including me. My father loved it. There are numerous sulfides in garlic. But this is likely complicated because some of these compounds exist as more complex precursor compounds and intolerance may be related to other enzyme systems.

A lot of people on the forums have as one of their many various odors a smell of burning rubber. Could this be a phosphorous compound ?
I think the compound smelled in burning rubber is a sulfur-compound based.

Quite a few in the group feel they have an allergy to penicillin. If this was rather to do with the DME's, could it be FMO3 deficiency ?
I think penicillin is a direct-acting allergen that is probably normally moped up but if someone doesn’t have adequate protein to protect then it reacts with key proteins that illicit an immune response. That is why it may be idiosyncratic. I don’t think it has much to do with DMEs or metabolic bioactivation. However, reaction to penicillin may indicate a more sensitive immune system.

Is smoking bad for someone with a FMO3 deficiency ?
Nicotine is an FMO3 substrate. It is only N-oxygenated about 5% of a dose but it is a detox pathway. Defective FMO3 will cause individuals to be more susceptible to nicotine. It may be that people with defective FMO3 may be more sensitive to the properties of nicotine.

Would it be impossible to follow a ‘low FMO3 substrate’ diet?
Due to the ubiquitous nature of amines and sulfides in the diet, it may be difficult to have a diet free of FMO3 substrates. However, one can try to avoid choline, for example and this may help a great deal. However, it is important to note that choline is essential in development and child-bearing age women need to consume adequate choline if they are contemplating pregnancy.

What do you think the results of this dissertation imply? http://digitalcommons.library.tmc.edu/dissertations/AAI1450285/
I did not read the dissertation but I did read the Abstract. I agree, more work needs to be done especially the role of non-exon mutations of FMO3.

Many people say they smell of many various smells systemically. We wondered if there is a possible FMO3 connection.
Yes, individuals reporting TMAu symptoms report various smells and this has been confirmed by other experts.

We wondered if the following were good FMO3 substrates ?
hydrogen sulfide: probably not
methanethiol: yes
dimethylsulfide: yes
dimethyldisulfide: yes. I believe it is a very good substrate.
ammonia: probably not
mercaptans: Yes, depending on the structure
Any others you wish to mention : Phosphines.

We wondered if the following things mainly in the diet or endogenously are FMO3 substrates ?
amines in diet
sulfurs in diet
phosphorous in the diet
selenium supplement
FMO3 substrates created endogenously
FMO3 substrates created by the gut flora (aside from trimethylamine)
methyls

It is difficult to answer a broad question like this without some specific examples.

There was a recent paper about FMO3 induction. http://www.ncbi.nlm.nih.gov/pubmed/20570689
Do you think it has any potential as a treatment ?

Not 3-MC. This also induces lots of other things and leads to liver cancer induction. I think induction FMO3 is not the real solution to TMAu. And note, in the report, the functional enzyme activity was not "induced" as much as the RNA.

It’s been suggested that Ataluren may be worth trialling for those with FMO3 nonsense mutations http://www.ptcbio.com/3.1.1_genetic_disorders.aspx. Do you think this is an option for investigation and what percentage with TMAU1 have nonsense mutations ?
Very very few individuals with TMAu in our analyses have nonsense mutations. I don’t think this is worth the risk.

A DME expert suggested ingestion of synthetic FMO3 may be theoretically possible but thought the side effects may make it unfeasible. What do you think of this idea ?
We are looking into this. There are many hurdles in this business. I am not sure about side effects of FMO3.

Is there any other ideas you have as potential treatments ?
I have lots of ideas but no money or time to pursue them.


tmau testing usa
MEBO RESEARCH STAFF




Sunday, July 4, 2010

tmau.org.uk interview with Nigel Manning: TMAU tester in the UK

tmau.org.uk have conducted an in-depth interview with Nigel Manning, the only clinical TMAU tester in the UK. Nigel is the Principal Clinical Scientist, Dept. Clinical Chemistry, Sheffield Children's Hospital. Nigel has already offered to help arrange testing for those who wish to test by writing to your doctor. He can also arrange testing through him for overseas readers as well.


Nigel is very sympathetic towards the body odor community, and has previously kindly given the blog an interview, as well as giving us an informative PDF about his testing procedure and results at his lab. He also allows those thinking of testing to contact him, as well as allowing people to ask for advice on their results

Nigel Manning email address : Nigel.Manning@sch.nhs.uk

Wednesday, February 17, 2010

'Microbes and Us' Slide presentation by Dr. Irene Gabashvili for MEBO Nashville Conference 2010



View more presentations from Aurametrix.
IN addition to having a good time doing our trial run of Dr. Irene Gabashvili’s presentation, ‘Microbes and Us’, in Vokle live, chat, real-time e-mail, she has now posted for everyone to see these slides and Q&A transcript of the Live Online Webinar, which took place on February 12, 2010. This transcript is very informative and particularly interesting as it identifies the normal bacterial flora of humans and where bacteria lives in our bodies, explains the types of microbes including intestinal microbiota responsible for IBS-C, IBS-D, IBD, Crohn’s disease, as well conditions that may be linked to microbiota, such as halitosis, hyperhidrosis, multiple chemical sensitivities, food intolerances (IBS, Celiac, TMAU, CFS), and more. Dr. Irene Gabashvili, Founder of Aurametrix, Personal Health Management Systems, presents an in-depth discussion of microbes including Pathogenic Bacteria DatabaseAlphabetical List of Pathogenic Bacteria’, which has one of the most complete database of the species. In this slideshow presentation, there is a section entitled ‘Diet Tidbits’ which addresses the most widely promoted prebiotics that have been suggested to increase the number of bifidobacteria and discusses the benefits of probiotics. This section also touches upon a very restrictive diet promoted as a way of reducing IBS symptoms, Crohn’s disease, Ulcerative Colitis and autism.
The final section includes the answers to the following webinar audience’s questions:

  • Why do people have Bacterial Overgrowth?
  • Do bacterial populations in human body depend on genetics, environment?
  • What kind of bacteria are TMA-producing?
  • I heard that Solobacteria causes halitosis. Is it really so? (includes a list of ‘Halitosis-related bacteria’)
  • What bacteria smell?
  • Is heterogeneity of metabolic body odor sufferers hindering research?
  • The collection of microbes for study must be a problem. Cross-contamination, etc.
  • How do you get them?
  • What is the most effective treatment to eliminate the desired bacteria: food or antibiotics?
  • How often can we take antibiotics without causing harm?
  • How does stress affect bacteria and enzyme deficiencies / pathways?
  • How does stress affect intestinal permeability?
  • Could a probiotic cleanse (sold on the market) help to flush us help to populate good bacteria?
  • For many of us the diet is confusing would it be difficult to customize a diet for us?
  • How long will it take to see diet results?
  • What would be the ideal diet..Are proteins beneficial?
  • Why some IBS patients have no odor while others do?
  • Can FMO3 be genetically engineered into a probiotic?
We would like to thank all the participants who asked these questions and to our Pharmaceutical Scientist and owner of body odor support.com, Arun Nagrath, for participating in our live discussion session. In spite of our technical ‘growing pains’ as we attempted to create this piece, all in all, we have acquired very valuable information from Dr. Gabashvili, to whom we are deeply appreciative for having helped us initiate this test webinar for the MEBO TMAU, Body Odor and Halitosis Webinar Series. We hope to hear much more from her as she has also so graciously volunteered to be the Overseer of MEBO Research’s exploratory study. On behalf of the body odor/TMAU and halitosis community, we thank you, Irene. http://aurametrix.com http://www.linkedin.com/in/igabashvili http://sites.google.com/site/irenegabashvili/ http://www.biology.sjsu.edu/facultystaff/gabashvili.aspx

Sunday, September 27, 2009

tmau.org.co.uk interview with Dr Robin Lachmann

Once again the tmau.org.uk website has come up with a notable exclusive in body odor and halitosis world. A while ago they said they would be interviewing Dr Robin Lachmann of the Adult Metabolism Unit in London and asked for readers to put questions to him. The interview has now been done and the result can be seen on the tmau.org.uk website.

tmau.org.uk interview with Dr Robin Lachmann about trimethylaminuria

The tmau.org.uk site is also in the process of getting together some tmau-diet meal plans which it will publish in the future. Thanks again tmau.org.uk and Dr Lachmann.

Tuesday, May 26, 2009

Shewanella baltica and other TMA producing bacteria in the gut


Nigel Manning
Principal Clinical Scientist
Dept. Clinical Chemistry
Sheffield Children's Hospital
Sheffield
email : Nigel.Manning@sch.nhs.uk


Excerpts from Part 2 of Interview with Nigel Manning
March 2009
The bacteria possibly responsible for the production of trimethylamine in the gut

Do we know what bacteria is responsible for gut Trimethylamine (TMA) production ?

NM: There are more than 400 species of bacteria in the colon but only a few described as TMA-producing. The fishing industry’s research microbiologists have published many papers on TMA and ‘fish-spoiling’ and cite species such as Vibrio harveyi, Vibrio fischeri, Photobacterium leiognathi and Shewanella baltica. The last of these is also know to generate hydrogen sulphide – or ‘ rotten egg’ gas. Whether these microbes are those responsible for human TMA production is a good question, but they may represent a small portion of the total.



[Shewanella baltica]...is also known to generate hydrogen sulphide - or 'rotten egg' gas.Shewanella baltica: Shewanella baltica (baltica of the Baltic Sea) is both an aerobic and anaerobic bacterium. Shewanella is the sole genus in the Shewanellaceae family of marine bacteria. Shewanella baltica are H2S-producing [hydrogen sulphide-producing] bacterial isolated from marine fish (mainly cod, plaice, and flounder) caught from the Baltic Sea. In aerobic conditions, the Black Sea strains of S. baltica absorbed significant quantities of Fe(III) from its medium, then reducing it to Fe (II) in anaerobic conditions. Under anaerobic conditions, S. baltica also oxidizes organic matter from the reduction of nitrate and sulfur compounds as well. S. baltica also has putrefaciens capable of high-rate azoreduction and humus reduction under anaerobic conditions. S. baltica produces a black precipitate of FeS when grown on TSI agar medium...(1)

Vibrio harveyi: Vibrio harveyi is a species of Gram-negative, bioluminescent, marine bacteria in the genus Vibrio. V. harveyi are rod-shaped, motile (via polar flagella), facultatively anaerobic, halophilic, and competent for both fermentative and respiratory metabolism. The do not grow at 4°C or above 35°C. V. harveyi can be found free-swimming in tropical marine waters, commensally in the gut microflora of marine animals, and as both a primary and opportunistic pathogen of marine animals, including Gorgonian corals, oysters, prawns, lobsters, the common snook, barramundi, turbot, milkfish, and seahorses[1]. V. harveyi is responsible for luminous vibriosis, a disease that affects commercially-farmed penaeid prawns[2]. Additionally, based on samples taken by ocean-going ships, V. harveyi is thought to be the cause of the milky seas effect, in which, during the night, a uniform blue glow is emitted from the seawater. Some glows can cover nearly 6,000 square miles. (2)

Vibrio fischeri: Vibrio fischeri is a gram-negative rod-shaped bacterium found globally in the marine environments. V. fischeri has bioluminescent properties, and is found predominantly in symbiosis with various marine animals, such as the bobtail squid. It is heterotrophic and moves by means of flagella. Free living V. fischeri survive on decaying organic matter (see saprotroph). The bacterium is a key research organism for examination of microbial bioluminescence, quorum sensing, and bacterial-animal symbiosis.(3)
See image results for Vibrio Fischeri (4)

Photobacterium leiognathi:
Since ancient times mariners have reported seeing glowing seas as their ships sailed through the night. More recently, satellites have recorded pictures of glowing seas off the eastern coast of Africa. The bioluminescent microbes responsible for such phenomena require specific conditions and high concentrations to achieve this effect, but it is similar to the algae blooms that cause red tide. There are many varieties of bacterium that can emit light, and some of them have developed symbiotic relationships with animals. Photobacterium leiognathi is one such species...(5)

References:
(1) http://microbewiki.kenyon.edu/index.php/Shewanella_baltica
(2) http://en.wikipedia.org/wiki/Vibrio_harveyi
(3)
http://en.wikipedia.org/wiki/Vibrio_fischeri
(4)
http://images.google.com
(5) http://web.mst.edu/~microbio/BIO221_2006/P_leiognathi.htm

Tuesday, March 24, 2009

Part 2 of interview with Cass Nelson-Dooley of Metametrix

The following is Part 2 of the interview with Cass Nelson-Dooley, Clinical Consultant at Metametrix, with contributions by Mr. Tony Hoffman

Part 1 can be read here


Gut-smells body odor

Are you amazed that there are people around who smell of gut smells?

Yes, I imagine that must be difficult to deal with. I would compare it to the example of eating garlic. The sulfur compounds from garlic are liberated by chopping and chewing and these sulfur compounds emanate from the mouth and even the skin for some time afterward.
What causes fecal smells? (i.e. what does feces actually smell of and why)

The smell of feces comes from short chain fatty acids (SCFAs) and bacteria like E. coli. All the SCFAs have strong smells. Butyric acid is an SCFA and it smells like feces and even like body odor. E .coli has more of a mousy odor.
Do you have a good idea what microbes in particular cause gas smells? Do you have any theories as to how someone could smell of gut smells through their pores/breath?

It is likely that bacterial overgrowth occurs in the small bowel and the products are absorbed and then emanate from the skin. I wouldn’t expect that the malodorous products would be absorbed from the colon. If someone has an overgrowth of Disulfovibrio, there may be a sulfur smell. If someone has an overgrowth of Pseudomonas sp., the smell may be sweeter (grape-like), but still sickly sweet. There is a whole group of sulfur-producing bacteria. Citrobacter freundii produces sulfur. Additionally, if the person suffers with maldigestion then food will undergo fermentation and this produces putrefactive compounds such as putrescine. While blood borne body odor is likely multi-factorial, at least for some patients, healing the bowel and cleaning up the diet could provide some relief.
Do you think with gut-related metabolic body odors, it's likely an enzyme is saturated? For instance a drug metabolizing enzyme? Any thoughts as to which one(s)? Any thoughts as to a scenario?

In addition to dysbiosis, I think it could be enzyme saturation or lack of vitamin and mineral cofactors. Metabolic diseases such as amino acidurias or organic acidurias have been characterized by strange odors, especially in the urine. These disorders occur due to lack of an enzyme, poor function of an enzyme, or low levels of cofactors causing the enzyme to malfunction. The result is too much of the byproducts, which can be smelly in high concentrations.
Does leaky gut mean 'leaky small intestine'? Do you think leaky gut or 'leaky colon' is likely a factor?

Leaky gut is often involved in cases of dysbiosis. It could be a factor in people with blood borne body odor, but I wouldn’t know for sure without an IgG4 food antibody test. Intestinal permeability, or “leaky gut,” has been implicated in inflammatory bowel diseases such as Crohn’s disease, non-alcoholic fatty liver disease, alcoholic liver disease, food allergy, acute pancreatitis, celiac disease, multi-organ dysfunction, and autism. According to the leaky gut hypothesis, genetic predisposition to poor intestinal barrier function, coupled with stressors such as NSAIDS or alcohol, can result in permeation of the intestinal mucosa. Antigens and bacteria are then able to cross the intestinal membrane and enter circulation where the immune system launches an attack against the antigens.
What kinds of tests would you recommend for a person suffering with blood borne body odor?

Without knowing a detailed history on the patient, I would recommend the GI Effects, the Organix, and the 40 amino acids. I recommend those lab tests because of the likely involvement of gut dysbiosis and abnormal SCFAs, vitamin need, and metabolic diseases involving amino acids and organic acids. I would also recommend IgG4 Food Antibody testing, especially if the person has gut, skin, or autoimmune symptoms.

Trimethylaminuria
Do you think a particular type of bacteria are responsible for gut trimethylamine production? Is it likely the same one thought to cause bacterial vaginosis (Gardnerella)?

Yes. The more smelly compounds like trimethylamine and hydrogen sulfide are not products of human metabolism, but they are produced by several bacteria under certain conditions. They tend to be strict anaerobes that could dwell in the colon or the vagina.
There is a 'diagnosis' of 'Secondary TMAU', where the enzyme involved is deemed fine, but the person has too much trimethylamine. Do you have any suggestion as to how to kill off the TMA-producing bacteria in particular?

The first thing to do is lower protein intake and improve protein digestion to reduce undigested nitrogenous substrates (amino acids) that must be present to form ammonia. Perhaps water or juice fasting could be beneficial in these instances as it can change the microbial content of the gut. If you don’t feed the colonic bacteria, they can’t grow and produce strange products.
Some feel that trimethylamine can produce a wide range of odors. Do you think trimethylamine could cause the wide range of gut smells on its own?

No. However it can be a component in complex mixtures of products that are responsible for the varying odors among individuals.

Final Questions
What do you think of the quality of probiotics on the market and are there any brands of probiotics you recommend ?

We are impressed with Klaire Labs probiotic and prebiotic formulas. I also like Custom Probiotics and a high dose probiotic called VSL#3. Designs for Health has a good probiotic product as well.
Is taking prebiotics on its own a good idea ? And which type of prebiotic do you feel is best ?

Fruits and vegetables are a great source of fiber (prebiotics). Other ideas are inulin, xylooligosaccharides, larch arabinogalactans, and beta glucan.
Is there general treatment advice for 'suspected' dysbiosis or does it vary too much ? For instance, take nystatin and metronidazole in a 'scorched earth' policy ?

I think the “4R Protocol” is the most general treatment advice and it’s comprehensive, but every doctor has a different approach and dysbiosis treatment should be tailored to the patient.

Treatment using 4 “R” Protocol for Intestinal Health from the GI Effects Interpretive Guide

Remove offending foods, medications, gluten (if sensitive) and reduce poor quality fats, refined carbohydrates, sugars, and fermented foods (if yeast is present). Consider antimicrobial, antifungal, and/or antiparasitic therapies in the case of opportunistic/pathogenic bacterial, yeast, and/or parasite overgrowth (see below for specific recommendations).
Replace what is needed for normal digestion and absorption such as betaine HCl, pancreatic enzymes, herbs that aid in digestion such as deglycyrrhizinated licorice and marshmallow root, dietary fiber, and water.
Reinoculate with favorable microbes (probiotics such as Lactobacillus sp., Bifidobacter sp., and Saccharomyces boulardii). To enhance the growth of the favorable bacteria, supplement with prebiotics such as inulin, xylooligosaccharides, larch arabinogalactans, beta glucan, and fiber.
Repair mucosal lining by giving support to healthy intestinal mucosal cells, goblet cells, and to the immune system. Consider L-glutamine, essential fatty acids, zinc, pantothenic acid and vitamin C.
Why does the intake of probiotics sometimes produce bloating and gas in some people and not in others?

Not all people react the same to probiotics because it depends on their microbial populations. When a person has a poor diet (high simple sugars, low fiber), taking probiotics can produce gas. However, this usually goes away with time. If the patient increases complex carbs and decreases simple sugars that often decreases any gas and bloating brought on by the probiotic. When there are unexplained reactions to probiotics or prebiotics, it is a good idea to run an Organix test, a GI Effects test, or food antibody test to identify underlying imbalances.

Part 1 can be read here

Monday, March 23, 2009

Interview with Cass Nelson-Dooley of Metametrix : Part 1

Gut dysbiosis is an unknown factor in systemic body odor and halitosis, although secondary TMAU (TMAU2) seems to mainly be accepted as meaning abnormal TMA-production from bacteria. However, most seem to feel they have a gut problem, and it seems there could be a connection, especially in gut-smells body odor.

One of the leading labs in testing for 'gut dysbiosis' and similar underlying problems, is Metametrix based in Duluth Georgia. They have recently pioneered DNA testing of microbes in stool samples, which means they can identify far more strains of bacteria than normal stool-culture testing. Their website is always worth a visit: Metametrix website

Cass Nelson-Dooley, M.S, Clinical Consultant at Metametrix Clinical Laboratory, has kindly given us an interview, with contributions by Mr. Tony Hoffman, on the work at Metametrix, and how it may apply to metabolic body odor and halitosis. Thank you Cass and Metametrix.

This is part 1 of 2
Part 2 is here


Metametrix questions
Intro and general questions
Would you like to summarise the history of Metametrix and what they do ?

The mission of Metametrix is to improve health worldwide by providing clinical laboratory tests that identify nutritional imbalances and toxicities underlying chronic diseases. Metametrix Clinical Laboratory has been around for 25 years, providing innovative laboratory tests to integrative clinicians. For example, we offer vitamin blood tests, fatty acid blood tests, and food allergy tests. Almost two years ago, we released a ground-breaking test, called the GI Effects, which measures stool bacteria, fungus, and parasites with DNA analysis. We are the first ones in the world to offer such a test.
How much do you think is known about the gut ecology and states of dysbiosis currently ? Is there more to discover?

I think that we have some good ideas about gut ecology and dysbiosis currently but there is always more to discover. The human GI tract is very long and our tools for measuring what happens in the GI tract are limited. For example, until now, it was very difficult to know what was happening with bacteria in the anaerobic (no oxygen) regions of the GI tract. Stool tests were done by culture, so environmental oxygen would make it very hard to grow and measure these “oxygen-hating” bacteria. I think new technologies such as RT-PCR will help us find out much more about the microbiota of the human GI tract.
Is the general rule for a symbiotic gut something like: a bit of lactobacillus in the lower small intestine, a lot of bifidobacteria in the right side of the colon, and non-carb type bacteria in the lower left?

I think Lactobacillus and Bifidobacteria have enjoyed all of the attention when it comes to healthy GI bacteria, mostly because these bugs can grow aerobically and can be packaged for sale. While the GI tract contains hundreds of different species, 30-40 species from only 5-6 genera make up 99% of the total biomass. Therefore, measuring the predominant genera offers a good snapshot of the colon environment. The anaerobic bacterial genera measured in the GI Effects test are those known to be present in humans: Bacteroides species (sp.), Prevotella sp., Fusobacteria sp., Mycoplasma sp., Clostridium sp., Lactobacillus sp., Bifidobacter sp., and E. coli. I think the more diversity of organisms, the better. Some studies show that as we age, the biodiversity of our GI bacteria decreases, making us more vulnerable to pathogens.
Is stool DNA testing likely to be as good as stool microbial testing will get?

I think DNA analysis in stool testing is an enormous leap forward in technology. In the Manual of Clinical Microbiology they state, “PCR is the best developed and most widely used nucleic acid amplification strategy…These techniques have sensitivity unparalleled in laboratory medicine, have created new opportunities for the clinical laboratory to have an effect on patient care and have become the new ‘gold standards’ for laboratory diagnosis of several infectious diseases.” With DNA analysis, we are seeing the microbial population with more sensitivity and specificity than ever before. Doctors and scientists trained on the older culture techniques have to view DNA results with a fresh perspective. I think that stool microbial testing will continue to evolve and improve in ways that we can scarcely imagine today.
You mentioned that in your GIfx results, there appears a trend of 3 clusters of dysbiosis? Could you elaborate on this?

Among the nine genera that we are measuring, some tend to grow together while excluding others. So, we are advancing our ability to discriminate one type of bacterial overgrowth from another. At this point, we do not know which cluster might be more associated with formation of malodorous products.
Are you finding parasites to be a common problem? Mainly protozoan?

We see parasites in about 18% of people. Some parasites are more common than others. Based on our in-house research the population data shows about 6% of people have Blastocystis hominis, 5.5% Necator americanus (or hookworm), and 5.3% Cryptosporidium.
How big a problem is candida in your results and would you like to make any comments about candida?

In the population that submits stool tests to us, we see about 12% Candida. This is less than observed by stool culture. According to our data that discrepancy is due to false overgrowth in transport media. We will publish more on this soon. We also assess the upper GI tract for Candida overgrowth using an excellent marker of Candida called D-Arabinitol. It can be measured in urine and there is a lot of research on this compound in blood as a measure of invasive candidiasis.
If someone has dysbiosis and a simple-carb addiction, would candida be the main suspect, or is there other usual suspects?

When someone has gut symptoms suggesting dysbiosis and a simple-carb addiction I try to be open-minded to other causes besides Candida. I think some people assume the patient has Candida when they actually have bacterial overgrowth. I’ve seen cases where the patient results show various bacteria species are very high and Candida is not an issue at all! I think the excessive bacteria can suppress the fungal growth. I also wonder about adrenal exhaustion and neurotransmitter status when people crave sugars. I think dysbiosis can often be a side effect of food intolerances. This is why laboratory testing is so important for doctors and patients. You can find out the cause of your symptoms instead of shooting in the dark.
How big a problem is poor digestive function in your results?

On the GI Effects test, we commonly see patients who show problems digesting fat, protein, or that have poor pancreatic function. Sometimes the clinician expects to find that the patient has a parasite due to abdominal pain and actually the pain appears to be caused by problems digesting and absorbing nutrients from the diet.
What type of symptoms would someone with over-dominant lactobacillus have and how common is it? Would taking Bifidobacter on its own always be ok?

It is possible to have too much of a good thing- namely Lactobacillus sp. Normally this occurs when people eat too many refined carbohydrates or if they’ve had a surgical procedure in the small intestine. A diet rich in simple carbs and poor absorption can feed the Lactobacillus. Similarly, alterations in the anatomy of the small intestine can create pockets where Lactobacillus can thrive. We measure Lactobacillus in the GI Effects Profile and also we look at the metabolite, D-Lactate in urine. I think treatment with a diet low in refined sugars, a probiotic (Bifidobacteria or Saccharomyces boulardii), and fiber, can help.
Does the Organix Dysbiosis urine test complement the stool test? Or could it be overlapping the same result?

The results of the Organix Dysbiosis Profile and the GI Effects Profile are used in conjunction to assess the health of the whole GI tract. The Organix Dysbiosis Profile is a urine test that measures bacterial and fungal by-products. These organisms are growing in the small intestine, where the by-products are absorbed and are present in the person’s circulation and eventually in the urine. In contrast, the stool results reflect the health of the colon. I also think a food antibodies test is useful when trying to see into a person’s GI health.