Analysis of odor-management products intended for hunting

“FORGET THE WIND.
JUST HUNT."

We know that animals have a more keen sense of smell than humans, and there is a market of products targeting hunters who wish to ‘mask’ their scent in order to get as close as possible to their prey without being detected.

This post neither endorses or discredits the benefits of these products, but only wish to present them to body odor sufferers with as thorough a description of their ingredients as available to us. This post will focus on the products on sale on the scentblocker.com website. It would be interesting to see if the concentration of the active ingredients in any of these products is strong enough for any type of uncontrollably strong body odor, and particularly a metabolic body odor.

It would be beneficial to the BO community if anyone who does try any of these products write a comment about their experience by clicking on the ‘Comment’ icon at the bottom of this post, and letting us know if it is potent enough to remove an uncontrollably strong body odor.

Robinson Outdoors almost single-handedly invented the category of scent elimination in the hunting industry back in 1985 with the development of Scent Shield ®. This was the very first product of its kind, intended to prevent deer and other big game from smelling human odor given off by hunters.

Since that introduction years ago, Robinson Outdoors has consistently led the way in scent eliminating innovation. New products were developed to help hunters get clean and stay scent-free. Products like Scent Shield® Clothes Wash and Body Soap were not just fragrance- free formulas; they contain ingredients that prevent the formation of odor in the first place.

These are some of the Scent Shield® products with a brief description of their ingredients. Anyone wishing to try these products is encouraged to write the manufacturer for additional information if concerned.

Carbon Blast $8.99 (16 and 32 ounces spray bottles)
Carbon Blast™ is one of the most revolutionary spray-on products ever developed for the elimination of human scent. Carbon Blast™ utilizes the incredible adsorption power of activated carbon. Carbon Blast™ chemically neutralizes and adsorbs human odor & other odors on hunting clothing, boots, caps, tree stands, fabric hunting blinds and related equipment, keeping it scent-free.

White Lightning™
Powered by a naturally occurring carbon-like compound, White Lightning™ is the newest innovation from the worldwide leader in scent elimination. Its ground breaking dual-action formula* chemically neutralizes and adsorbs odors, enabling hunters to get incredibly close to their quarry without being detected. White Lightning™ is recommended for boots, clothing and equipment, and is incredibly effective wet or dry. Available in 12 and NEW 22 ounce bottles.

TI4™ Titanium ($15.99)
Utilizing the incredible power of Titanium
• Even works on more difficult odors
– ammonia, gas and other VOC’s (volatile organic compound), sulfides, smoke.
• Always on – works until the material is eventually washed or scraped away.
After it is applied and the moisture evaporates, a residual of Titanium Dioxide remains.
• Non-toxic, environmentally friendly Titanium Dioxide produces Hydroxyl radicals, which are powerful oxidizing agents that react with the organics found in odors – reducing them to harmless, odorless compounds.
• Retains these properties even after washing.

NEW Revolutionary Quad-Action Scent Eliminator
1. Prevents odor from forming in the first place - NO Gas, NO Odor
2. Adsorbs human and other alarming odors you may encounter
3. Neutralizes human odor on contact and well after it is dry
4. Oxidizes tougher odors by breaking them down


Body Shield™ Deodorant Pill
• Eliminates odor internally, utilizing Chlorophyllin Copper Complex.
• High potency Parsley and Alfalfa powder concentrate* helps control mouth odors.
• Safe internal deodorant reduces human waste odors.

*NOTE: Although this may contain Chlorophillin Copper Complex, it may not be recommended to persons on a low choline diet.
* 100 grams of dried parsley contains 97.00 mg of choline, and
*100 grams of Alfalfa seeds (not powder) have a total of 14mg of choline

http://www.scentblocker.com/osc/about_us.php

TMAU story on Discovery Health : Mystery Diagnosis, The boy who stopped walking

Thanks again to Cheryl, who again has boldly allowed her trimethylaminuria story to be told to the media, with the beneficiaries being all metabolic body odor and haltiosis sufferers. She truly is a brave pioneering soul.

Cheryl also founded the charity research fund for TMAU at NORD. The 'donate online' instructions are unclear as to how you donate to TMAU research in particular, although it's likely if mentioned that it will go to TMAU. This needs to be clarified.

The program on TMAU was part of the Mystery Diagnosis series

channel: Discovery Health
series : Mystery Diagnosis
episode: The boy who stopped walking

Obviously it must be the second half of the episode. Discovery Health say that previous episodes can be bought on Itunes, though presumably this is only the audio. The program includes comment from Dr Fennessey of the University of Colorado Denver Health Sciences Center. He could be regarded as instigator of trimethylamine urine testing in the USA. His lab is one of the few in the USA, and probably tests the vast majority of samples (90%+ ?)

Thanks again to Cheryl, brave pioneer.

2 minute hypnosis by Wendi Friesen

http://www.youtube.com/user/WendiFriesen

New TMAu pubmed paper from HBRI

published 2009 Feb 27

Novel variants of the human flavin-containing monooxygenase 3 (FMO3) gene associated with trimethylaminuria

Motika MS, Zhang J, Zheng X, Riedler K, Cashman JR.
Human BioMolecular Research Institute, 5310 Eastgate Mall, San Diego, CA 92121, USA.

The disorder trimethylaminuria (TMAu) often manifests itself in a body odor for individuals affected. TMAu is due to decreased metabolism of dietary-derived trimethylamine (TMA). In a healthy individual, 95% or more of TMA is converted by the flavin-containing monooxygenase 3 (FMO3, EC 1.14.13.8) to non-odorous trimethylamine N-oxide (TMA N-oxide). Several single nucleotide polymorphisms (SNPs) of the FMO3 gene have been described and result in an enzyme with decreased or abolished functional activity for TMA N-oxygenation thus leading to TMAu. Herein, we report two novel mutations observed from phenotyping and genotyping two self-reporting individuals. Sequence analysis of the exon regions of the FMO3 gene of a young woman with severe TMAu revealed heterozygous mutations at positions 187 (V187A), 158 (E158K), 308 (E308G), and 305 (E305X). Familial genetic analysis showed that the E158K/V187A/E308G derived from the same allele from the mother, and the E305X was derived from the father. FMO3 variants V187A and V187A/E158K were characterized for oxygenation of several common FMO3 substrates (i.e., 5- and 8-DPT, mercaptoimidazole (MMI), TMA, and sulindac sulfide) and for its thermal stability. Our findings show that with the combination of V187A/E158K mutations in FMO3, the enzyme activity is severely affected and possibly contributes to the TMAu observed. In another study, genotyping analysis of a 17year old female revealed a mutation that caused a frame shift after K415 and resulted in a protein variant with only 486 amino acid residues that was associated with severe TMAu.

http://www.ncbi.nlm.nih.gov/pubmed/19321370

Comment:
This is a new paper on FMO3 genetics in relation to trimethylaminuria, by the staff at the HBRI genetics lab in San Diego, one of the few labs in the world known to be researching FMO3 genes, amongst other genes. It's not clear the reason for the study (2 case studies). The words in bold are to emphasise possible important points.

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related links:
HBRI staff
HBRI page on trimethylaminuria and testing through HBRI (both DNA and urine)
Volunteer table of known FMO3 mutants, run by Dr Shephard in London
Videos on basics of genetics

De-Fishing Soap

The De-Fishing Soap : Is it good for TMAU sufferers?

There are many skin products in the market that persons with odor need to cipher through to determine what will work and not work to help reduce fish odor produced by a deficiency in the FMO3 enzyme. After running across this video on De-Fishing Soap, I decided to research a little more into it. I think it’s important that sufferers become informed consumers.

After reading the ingredients of this soap, I see that it contains glycerin. It so happens that glycol concentrate (Propylene Glycol) has a pH of 9.5, as indicated in a chart in raypak.com . In another site, peacefulscents.com, I found these beautiful soaps that also contain glycerin which they claim has a very high pH of 8 to 9.

Soaps with such high pH seem to go against the research posted in this blog, one of which basically quotes a Trimethylaminuria paper written for the NIH Gene Reviews, sited by Drs. Phillips/Shephard in London,

Use of acid soaps and body lotions. Trimethylamine is a strong base (pKa 9.8). Thus, at pH 6.0, less than 0.02% of trimethylamine exists as the volatile free base. The use of soaps and body lotions with a pH close to that of normal skin (pH 5.5-6.5) helps retain secreted trimethylamine in a less volatile salt form that can be removed by washing.

This paper recommends the use of acid soaps and body lotions to reduce the very alkaline pH of TMA. Another paper by the University of Washington, Seattle, funded by the National Institutes of Health, also recommends the use of acid soaps and body lotions.

Therefore it appears that the De-Fishing Soap works well only for fishermen whose source of fish odor is an external source. It may be that the star anise essential oil and the Australian tea tree essential oil could work well with the glycerin to remove the TMA smell of the fish. However, the TMAU sufferer’s fish odor comes from an internal source - the TMA flowing through the blood and coming out of the skin through perspiration. Therefore, a person with TMAU have different needs, which are primarily to lower the skin's pH.

These are the ingredients of this soap:

De-Fishing Soap contains purified water, glycerin, sodium stearate, sorbitol, propylene glycol, Sodium laureth sulphate, stearic acid, lauric acid, sodium chloride, star anise essential oil, Australian tea tree essential oil, and FD&C blue dye #1

http://www.defishingsoap.com/

Research ideas for MeBO Research and the group

MeBO Research will be focusing on encouraging research into metabolic body odors and halitosis. Probably moreso 'fecal body odor' syndrome, since this seems by far the most common ... and possibly if that is solved then many more will be too. Naturally it will include TMAU, since this is the only generally recognised metabolic body odor. Dimethylglycinuria has one medical paper with such a diagnosis, and some TMAU testers do test for this too, but does not seem to have gathered 'momentum' as a diagnosis. Perhaps the DMGU paper was more useful for proving that if they look for smelly molecules with an open-mind rather than only trimethylamine, they might find other odorous volatile organic compounds.

The purpose of this post is to get people thinking about ideas for research. It's important that everything is transparent so that it may help others come up with their own ideas or instigate their own inquiries. The aim is to get us all smell-free as soon as possible, wherever the 'cure' comes from.

A few ideas MeBO will be asking around about initially are :

TMA-testing paper for home monitoring of trimethylamine:
The same as current urine test papers for ph/diabetes etc. This technology seems to already exist, but nobody is marketing it. For those who feel trimethylamine is their only source of odor, it would seem possibly helpful in monitoring the level of TMA at home.

FMO3-enriched probiotic:
Although FMO3 seems to be mostly situated in the liver, the trimethylamine is only produced in the gut. So you would think it may be possible to genetically engineer a gut bacteria to be rich in FMO3 enzyme and detoxify the TMA on site in the gut. This concept seems to be already available, and studies have been done using engineered-probiotics especially for hiv (click here) and crohns disease (and possibly others). Inquiries will be made about this. Again, quite possibly the only reason it isn't already done is because of lack of interest in the medical system and government regarding TMAU. Since FMO3 deals with a lot of smelly substrates (sulfides, amines and phosphorus compounds), you would think this idea may cover a lot of common smells sourced from the gut like fecal body odor. There has even been speculation a bacteria could be used to allow FMO-bacteria to circulate systemically. The concept has been mentioned in TMAU literature for a while.

As to the future, one may envisage some new approach to treating or managing the condition quite apart form the obvious one of gene therapy with replacement of the human gene for FMO3. Alternative approaches might embrace the following: use of gut absorbents, such as charcoal or ion-exchange resins; modify the gut flora to reduce the bacterial species responsible for the conversion of precursors to trimethylamine; incorporate micro-organisms "engineered" with human FMO3 into the gut flora, to oxidize any trimethylamine released to its non-odorous N-oxide; provide riboflavin supplements, a precursor of the FAD cofactor for flavin monooxygenase function, in an attempt to maximize any residual activity; and finally, from the cosmetic point of view, the development of "malodor suppressants" in hygiene products to disguise the offensive smell of trimethylamine.
Mitchell/Smith TMAU paper 2003

Speculative tests for profiling:
The only test on offer to smelly people is the TMAU test and perhaps the DMGU test. One should probably regard the medical system and governments as not interested in metabolic odor problems and perhaps we are in a situation where we should be trying to get a 'test profile' of the problem ourselves. For instance, very often sufferers suggest they have gut-type issues (especially in fecal body odor). It's probably a mistake to wait for the system to come up with answers for us. Although this option would be trial and error, some specificity 'guesstimates' could be made in deciding what areas to start testing, and who knows what the end results would be. There's a good chance fecal body odor is often a 'syndrome' with a few factors,judging by how a size-able % of sufferers seem to develop the problem well over 30. In a perfect world a government-initiated body odor and halitosis research center would be doing this type of research, as they did with a smell and taste clinic and other disorders. We need real data.

Other ideas:
Petition politicians

These are only some opening ideas that MeBO Research may be following, but since the 'goal' is for all of us to be smell-free, these ideas are by no means 'copyrighted' and more ideas are welcome.

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

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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.

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

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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.

An Interpretation of the Nigel Manning interview : part 1

We are grateful to the recent interview Nigel Manning, the main tester of TMAU in the UK, gave to the blog recently. It greatly helps the sufferers in our understanding of the issue.

The interview can be read here

It is important that body odor sufferers are aware of the testers out there, as well as their testing procedures, influences, and thoughts on the subject. Since so few labs test for TMAU worldwide, it seems they may not have an internationally agreed test protocol. This is the first in a series of posts about the interview, in an attempt to make sense of what was said (to fully absorb the information)

These posts will be an attempt to analyze the interviews and try and fully absorb what was said. Clinical science in it's early stages can be very subjective, and you could say TMAU testing is at a very early stage of it's development (until governments realise how common it is and set standards). Anything that can be clarified later on will be corrected.

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Trimethylaminuria Test Range
Nigel Mannings test range seems to be :

The ‘normal’ ranges were established early on by asking for volunteers (from the staff here at the hospital). TMA is regarded as normal if the concentration is below 11 micromoles per millimole of creatinine. TMA-oxide’s normal range is below 147 and the ratio of TMA to TMO is normal below 0.21.

TMA = trimethylamine
TMO = trimethylamine-n-oxide (the normal odorless metabolite)

Mr Manning seems to have defined the range levels himself (?), although it is clear he is well-read in TMAU medical papers. The normal concentration of TMA-creatinine is set at 11, whereas in 2 other TMAU papers the setting was around 18

Most individuals (with normal TMA N-oxidation capacity) excrete >95% of the combined TMA/TMANO load as TMANO or have a urinary TMA concentration of <18 http://www.ommbid.com/OMMBID/the_online_metabolic_and_molecular_bases_of_inherited_disease/b/abstract/part8/ch88.1

Concentration of unmetabolized TMA in the urine. A urinary concentration of free TMA of 10µg/mL (18-20 µmol/mmol creatinine) or higher, correlating with a urinary output of TMA of about 15 to 20 mg/day, appears to represent a threshold for the presence of the fishy body odor associated with the disorder [Mitchell & Smith 2001].
http://www.ncbi.nlm.nih.gov/bookshelf/br.fcgi?book=gene&partid=1103

Mr Manning also seems to include high TMA-n-oxide levels as indicative of TMAU, whereas it is unclear if others do this, since TMA-n-Oxide is the odorless final metabolite. Presumably such a condition (high TMA-n-o) would be part of his diagnosis of the 'secondary TMAU' spectrum, since it is clear TMA was metabolized at least.

The Sheffield lab is well-known as being possibly the only lab where forum posters on english-language body odor forums indicate they were positive for TMAU2. TMAU2 is generally accepted as existing, so the question is more a case of why no-one seems to be positive for this elsewhere ?

Substrate overload of FMO3 enzyme activity resulting from either an excess of dietary precursors of TMA or variations in gut fauna, causing increased release of TMA. This type of trimethylaminuria is characterized by a high concentration of TMA in the urine, but a normal urinary TMA/TMA N-oxide ratio.
http://www.ncbi.nlm.nih.gov/bookshelf/br.fcgi?book=gene&partid=1103

'Over the counter' celiac home test in the UK and NZ

The freedom to test is something very helpful to conditions such as metabolic body odor and halitosis, where sufferers are likely dismissed by doctors as wasting time, and so don't manage to get tested at all. Someday anyone will be able to pay for any test, and then you can say peoples own health is in their own hands. At the moment the government bodies are in charge of our health ultimately.

In the UK (and New Zealand, as far as we know), one helpful test that is now available over the counter (or on the internet) for a fee is a reliable(?) home test for celiac. While celiac does not cause metabolic body odor (e.g. fecal body odor), it probably makes sense for someone with fecal body door to look for anything that may contribute to a dysbiotic condition of the gut (until the day the government says : the body odor and halitosis clinic we ordered to be set up has now shown what causes fecal body odor and these are the factors of the syndrome).

The gold standard test for celiac is a biopsy, but there are a collective group of blood tests that are normally used since they are easier and also collectively are almost certain to be specific and sensitive for almost every case.

The group of tests are :

• Serologic Tests

1. EMA (Immunoglobulin A anti-endomysium antibodies)
2. AGA (IgA anti-gliadin antibodies)
3. DGP (Deamidated gliadin peptide antibody)
4. tTGA (IgA anti-tissue transglutaminase

the AGA and EMA tests are now probably considered outdated and unreliable outdated. The 'vital' new test nowadays seems to be the transglutaminase test.

The celiac sprue association website says :

Deamidated gliadin peptide (DGP) antibodies tests developed in 2007 in combination with Tissue transglutaminase (TTG) antibodies and have better accuracy than native gliadin antibodies. Multiplex immunoassay (MIA) measures multiple antibodies simultaneously providing with reduced turnaround time and cost. This test for antibodies is as accurate as ELISA for the presence of celiac disease. Rational combination testing can help identify patients who need intestinal biopsy.

Anibiotech of Finland have developed a home test that detects transglutaminase reaction. The test can be done in the form of a finger-prick test at home. If it is negative you cannot be totally sure you don't have celiac (false negative), but if you are positive it's very likely you have celiac. The person could then go on to test through their Dr.

If nothing else, it's a cheap way of at least ruling out something that is likely to be detrimental to your health, if not the reason for smelling.

Update: The Biocard celiac home test seems to be now available in the USA and other countries:
Example seller of Biocard Celiac test in USA

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Manufacturers of Biocard
example of an online seller in the UK

BBC video : laser sweat ablation (LSA) for axillary hyperhidrosis

While the blog is about metabolic/systemic/bloodborne body odor and halitosis, anything to do with body odor in general is worth mentioning. Some feel their problem is 'traditional' external body odor, so it was thought this may be of interest to them. In no way is this a recommendation of the surgery.

It is a video on the BBC news site about a new (in the UK) surgical way of destroying the sweat glands under the armpits.

http://news.bbc.co.uk/1/hi/health/7939141.stm

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related links
http://www.thewhiteleyclinic.co.uk/
Mark Whiteley's specific site on hyperhidrosis surgery at the Whiteley clinic

The Australian TMAU Foundation 2nd Newsletter

Rob Brown is a well known Australian TMAU sufferer, especially on the Yahoo TMAU Forum. He has taken the initiative and started the Australian TMAU Foundation charity, which aims to help in research into TMAU. The website is currently being constructed at http://www.tmaufoundation.org.au/index.html

The 2nd e-newsletter has just being released, and includes intriguing information on research, as well as an emotional (and typical) story of a sufferer.

There is mention of 2 possible lines of research in Australia, and also it appears that the main TMAU tester in Australia (probably the Brisbane tester) only tests for Trimethylamine levels, and not Trimethylamine-n-oxide levels (the final product of correct FMO3 metabolism of TMA).

As Dr Christodoulou points out

[I]t should be remembered that excessive trimethylamine excretion may be intermittent, so a normal single result does not rule out the disorder. The diagnosis can be more firmly established by conducting a choline or marine fish load test, or by FMO3 mutational analysis. Currently, there is only one laboratory in Australia offering biochemical testing for trimethylaminuria,but we believe this is suboptimal because this laboratory does not routinely quantitate trimethylamine-N-oxidase, potentially missing cases of the disorder. Best practice guidelines suggest that both trimethylamine and trimethylamine-N-oxidase should be measured.

Part 2 of interview with Nigel Manning

This is part 2 of an email interview with:

Mr Nigel Manning, Principal Clinical Scientist
Dept. Clinical Chemistry
Sheffield Children's Hospital
Sheffield

email : Nigel.Manning@sch.nhs.uk

Almost every patient TMAU urine sample in the UK will have been tested by Mr Manning.

Part 1 can be read here

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

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.

Is the bacteria in the colon or small intestine ?

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.

Do you think if someone has excess TMA, it could indicate that their gut flora is abnormal ? For instance small intestine bacteria overgrowth ?

[see previous answers]

Is there a particular antibiotic/treatment you think may be best to control excess bacteria in Secondary TMAU ?

[see previous answers]

Do you have any advice to Primary TMAU sufferers ?
Any advice to Secondary TMAU sufferers ?

To both of these questions I would recommend seeking the advice and guidance of a metabolic physician who specialises in TMAU – such as Robin Lachmann at The National Hospital for Neurology and Neurosurgery in London. There are several other metabolic specialists across the UK with increasing experience of TMAU, supported by dieticians, who can help TMAU sufferers with a variety of treatments from antibiotics and dietary regimens to odour-reducing tablets and low pH skin creams.

Do you think a Secondary TMAU diagnosis means in theory they should be able to be 'cured' ?

Yes, with the correct antibiotic therapy a patient with normal FMO3 activity but an overproduction of TMA by gut flora may be effectively cured.

Do you expect Primary TMAU positives to have problems with other FMO3 substrates ?

FMO3 may have up to 1000 substrates ie compounds that can be oxidized by this enzyme in the liver. With deficient oxidation these compounds may stay in the body longer and have unwanted consequences. Many drugs may be included in this list and are currently know to include codeine, tamoxifen, ketoconazole, nicotine, cimetidine, ranitidine and phenothiazine. High blood pressure is also a known complication due to foods which contain large amounts of the neurotransmitter tyramine (cheese, red wine and chocolate are examples). FMO3 deficiency should be taken into account whenever drugs are prescribed in case of an adverse reaction.

Do you think with Primary TMAU, the person may have other health weaknesses, such as chronic fatigue ?

It’s not possible to speculate about this – TMAU1 sufferers are individuals prone to conditions that all of us may encounter. Adverse reactions to FMO3 substrates may add complications under certain circumstances, such as hypertension (high blood pressure).

Many people, including people with primary or secondary TMAU diagnosis, as well as those who are negative, have wide ranging odors. From gas/fecal to rotten egg and all sorts. Do you have a theory on this ?

Body odour is caused by the release of volatile compounds from the skin in sweat. Just as TMA is produced in the gut by bacteria, there are probably many other volatile compounds which are naturally produced – like skatole which has a faecal odour. Only when the production of these compounds are produced in excess that the odour can become a problem. There may be other conditions like TMAU which are caused by an unusual gut flora as well as a lack of a detoxifying enzyme. Unfortunately we only have the ability to test for TMA at the moment.

Do you think with a TMAU diagnosis, they will only smell of 'fish body odor' ?

It may be possible to be afflicted with overproduction of more than one volatile compound if conditions in the gut are such that excesses of different species of odour-causing bacteria are pre-dominant. Other bacteria may be responsible for a mixture of volatiles. Some species of Shewanella are known to produce both TMA and hydrogen sulphide (rotten egg gas).

Are there any recent advances in TMAU ?

I’m not aware of any major breakthroughs in the treatment of TMAU, although as with many areas of medicine change is gradual and new therapies may be some time in development. Riboflavin treatment to boost the activity of FMO3 was mentioned a few years ago, although I’ve yet to see the results of any trial published.
Our advances in diagnostics have been in establishing a DNA service here at Sheffield Children’s Hospital. Recent increased awareness of the condition can certainly count as an advance – with it comes the prospect of increased chances to diagnose and treat TMAU sufferers.

What do you think sufferers could do to get research going ?

Perhaps by joining organisations such as the TMA Foundation (based in New York and ably run by Sandy) TMAU sufferers could channel efforts into fundraising to support researchers in the field of FMO3 function or antibiotic therapy trials.

Do you think it may be feasible for a manufacturer to develop a 'home
maintenance' TMAU test like they have for diabetes ? whether its TMAU test strip papers or a breathalyzer etc ?

There have been attempts at measuring TMA in sweat, although this is a long way from a commercial kit as a mass spectrometer was still required to detect the TMA.
When it comes to future developments – ‘never say never’ may be the best answer I can give.

Are there any ideas you have of possible 'money no object' lines of
research, such as genetic engineering ?

There are many hundreds of genetic conditions for which genetic engineering still remains the ultimate goal. Stem cell therapy with the correction of an abnormal gene, its re-introduction to the body and then normal function of the previously deficient enzyme may be possible in the future for many of these disorders….maybe even FMO3 deficiency.

Interview : Nigel Manning : The tester of almost all TMAU urine samples in the UK

The following is part 1 (of 2 parts) of an email interview with:

Mr Nigel Manning, Principal Clinical Scientist
Dept. Clinical Chemistry
Sheffield Children's Hospital
Sheffield

email : Nigel.Manning@sch.nhs.uk

Almost every patient sample in the UK (including by 3rd parties such as medichecks and The Doctors Laboratory) for Trimethylaminuria (urine test) will be tested by Nigel Manning at the Sheffield Children's Hospital. His hospital is also the only patient TMAU genotype tester (the DNA test) in the UK. We are very grateful to Mr Manning for his co-operation and all the work he does.

Part 2 is here

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Could you tell us a bit about what you and your lab's role is, and is TMAU testing only part of your work in the lab ?

I work for the Department of Clinical Chemistry at Sheffield Children’s Hospital where we provide a 24 hour diagnostic service for children at the hospital as well as specialized services for both our hospital and others from all over the country. Our specialty is the field of inherited metabolic disorders or inborn errors of metabolism. These are a wide ranging group of diseases which can present from birth to adulthood and have a genetic basis, so our field is often also known as ‘Biochemical Genetics’. We use a variety of techniques to identify and quantify biomarkers to diagnose disorders and hopefully lead to successful management of life-long conditions. We also provide prenatal testing for some of the most severe disorders.
My particular role is the development and running of tests by mass spectrometry, either coupled to another device known as a gas chromatograph (GCMS) or using an instrument known as a tandem mass spectrometer (MS/MS). My work measuring TMA has been developed over the years using GCMS. Originally the TMA test was carried out on an instrument which required me to manually inject the vapour taken from above a heated urine sample directly into the mass spectrometer, a technique known as ‘headspace’ sampling. Fortunately I now use a much more automated system which allows me to load prepared samples in special vials and let an automatic sampler introduce the headspace samples into a more modern GCMS.
TMA testing represents about 5% of my workload in the laboratory.

How did your lab come about testing for TMAU ?

Before 1997 we used to send our TMAs to a research lab for analysis, but their grant funding ran out so the service was withdrawn. At the time I had an idea for a method using our existing mass spectrometer. Fortunately when I experimented with this method of directly injecting headspace vapour into the mass spec, it worked. By adding a stable isotope of TMA to samples it was possible to measure TMA by monitoring the ratio of the patient’s TMA to the isotope. A published method provided more detail of how to measure both TMA and TMA-oxide (TMO) in a sample and this formed the basis for a TMA service.
In 2007, our colleagues at Sheffield Molecular Genetics Service set up a pilot project to look at mutations in the FMO3 gene in a group of UK TMAU patients. This quickly transferred to a diagnostic service that now complements the biochemical testing.

What are your TMAU testing 'parameters' and who set them ? (e.g. what reading constitutes a fail ? what constitutes Secondary TMAU ?)

The ‘normal’ ranges were established early on by asking for volunteers (from the staff here at the hospital). TMA is regarded as normal if the concentration is below 11 micromoles per millimole of creatinine. TMA-oxide’s normal range is below 147 and the ratio of TMA to TMO is normal below 0.21.
SecondaryTMAU is a very broad term, but essentially relates to any TMAU where normal TMA oxidation appears to be indicated. Increased TMA and TMO are usually markers for TMAU2, however we have seen TMAU1 patients (with proven FMO3 enzyme deficiency by DNA mutation analysis) whose samples also showed this pattern – albeit only temporarily. This makes the differentiation between TMAU1 and TMAU2 difficult without more than one sample to assess and without DNA analysis to confirm a mutation for the FMO3 gene.
In general – if the TMA is consistently increased the patient has TMAU.

Do you use a choline challenge ?

Some doctors who send me samples prefer to use a choline challenge as a good way of diagnosing TMAU. Choline itself is sometimes difficult to obtain for medical purposes and so dietary challenge is used. Fish and beans are useful, although marine fish contain high amounts of TMO so this may, if absorbed by the intestine, result in a high urinary TMO. As a laboratory scientist I don’t see patients but if a doctor asks me what constitutes a good choline challenge I would suggest 2 eggs with baked beans (420g). Soya beans and liver are other good sources of choline.

With regards samples already tested, do you know how many you have tested and how many were positive for Primary TMAU and how many for Secondary TMAU?

Over the last 10 years I’ve analysed over 919 samples from people who complain of an odour. To date 306 patients have shown significantly raised TMA (ie TMAU) with 201 showing a raised TMA/TMA-oxide ratio (possible primary TMAU) and 106 with a normal ratio (possible secondary TMAU).

Has there been an increase in testing ?

Yes, in 1998 I received 13 TMA requests and in 2008 there were 214. Increased publicity through a BBC3 TV documentary in 2007 may account for a dramatic rise as in 2006 requests numbered just 81.

What advice do you have to anyone having difficulty being authorized for testing by their G.P. ?

I can send a letter or email to any enquirer explaining the test and giving some background information about TMAU. Hopefully this information they can show to their GP who can phone me if they need more information. Obviously I must respect the professional opinion of any GP, but as I cannot accept any samples without an official request, the patient may wish to seek another primary care practitioner if they can’t get tested through their current GP.

Do you think someone could repeatedly pass the urine test but still have TMAU in practice ? (e.g. the DNA result predicts Primary TMAU)

This can happen in circumstances when a TMAU sufferer experiences a fluctuating or occasional odour, as in the milder TMAU cases and those who are genetic ‘carriers’ for TMAU1 (FMO3 deficiency). Dietary load and hormonal changes such as experienced during menstruation are known to result in a temporary but significant odour. TMA testing outside this time produces completely normal TMA result. It’s important to test for TMA when the odour is at its strongest – so timing of the sample collection is very important. Anyone with a periodic odour must wait until the odour occurs to collect some urine (preferably over 24 hours) or use a choline challenge before collecting a sample.

Secondary TMAU only seems to be tested in the UK that we know of. Why do you think this is so ?

Secondary TMAU or TMAU2 has been recognized for many years, although much of the TMAU interest has been in the inherited metabolic disorder FMO3 deficiency ie TMAU1. Very early on in the TMA service I received a urine from a pre-school age boy who was very odorous after eating fish. This was especially problematic because fish fingers were his favourite food and his parents had to persuade the parents of his friends to not serve fish fingers at birthday parties. The prospect of this going on when he started school was worrying, but after finding out about TMAU the parents arranged for the test to be done here. When I saw the very high TMA and TMO I suggested to the GP that a short course of the antibiotic metronidazole might help. After this dose this 4 year old had no more problems and could enjoy fish and chips with his family with no resulting odour – and still does ten years on. His TMAU had been cured and it convinced me that TMAU2 was an important part of the differential diagnosis.
TMAU2 from overproduction of TMA by bacterial overgrowth can be experienced for many years but if the correct antibiotic therapy is applied, can be cured by eradication of the bacterial responsible. Testing for TMAU1 or 2 is essentially the same, but results can usually differentiate one from the other. As I mentioned before there have been several occasions when a patient with marked increases in both urinary TMA and TMA-oxide (a TMAU2 pattern) then tests positive for TMA but with normal TMA-oxide (a TMAU1 pattern). This is why the DNA follow-up is so important.

Is someone keeping a database of the test results (UK/World) including DNA testing ?

Not to my knowledge.

Do you think there are many more FMO3 mutants/polymorphisms to be discovered?

Most genetic conditions have seen an ever expanding number of mutations discovered, so I would expect the same for FMO3 deficiency. The DNA testing here looks at the whole FMO3 gene and is estimated to detect >95% of mutations, though the number of studies carried out is relatively small.
There are certain mutations/polymorphisms that are more common in the population, and so these tend to account for most cases of TMAU1.

Have you's discovered any novel mutants/polymorphisms ?

No – my geneticist colleagues in our hospital have been testing for just 2 years, so it’s early days yet. So far, all the mutations found have been seen in other TMAU1 patients.

Do you think Primary TMAU may not be just an autosomal recessive problem ?

As far as is known, FMO3 deficiency has always been shown to be an autosomal recessive condition, though mild or intermittent symptoms can sometimes occur in carriers of FMO3 mutations.

Part 2 is here

2008 paper on neuronal processing of body odor

Functional neuronal processing of body odors differs from that of similar common odors

Lundström JN, Boyle JA, Zatorre RJ, Jones-Gotman M.

Department of Psychology, McGill University, Montreal, QC, H3A1B1, Canada. jlundstrom@monell.org

2008 paper on the neuronal processing of body odor

At the moment, the reason why most people can't be smelt by some people is wide open to theories. This seems to include 'classic' external body odor (armpit body odor), rather than just metabolic body odor (where it seems to be mostly the norm).

The olfactory system seems to be the least understood sense, and so no answers seem forthcoming soon. The main areas of theory would likely be around the olfactory system itself, or that some 'non-smellers' carry the same toxins in their circulating system themselves, and so there may not a wide enough 'detection gap'. Who knows ?

On a similar note, recent research by a group of Swedish scientists (psychologists) came up with the conclusion that the olfactory system 'learns' neural pathway patterns, and recognises 'friends' 'body odor' (presumably the non-detectable type ?) and feels safe, whereas new peoples 'body odor' stimulates fear (?)

Visual and auditory stimuli of high social and ecological importance are processed in the brain by specialized neuronal networks. To date, this has not been demonstrated for olfactory stimuli. By means of positron emission tomography, we sought to elucidate the neuronal substrates behind body odor perception to answer the question of whether the central processing of body odors differs from perceptually similar nonbody odors. Body odors were processed by a network that was distinctly separate from common odors, indicating a separation in the processing of odors based on their source. Smelling a friend's body odor activated regions previously seen for familiar stimuli, whereas smelling a stranger activated amygdala and insular regions akin to what has previously been demonstrated for fearful stimuli. The results provide evidence that social olfactory stimuli of high ecological relevance are processed by specialized neuronal networks similar to what has previously been demonstrated for auditory and visual stimuli.

2008 paper : Stephen Mitchell on FMO enzyme

Mitchell SC.
Biomolecular Medicine, Faculty of Medicine, Imperial College London, South Kensington, London.

http://www.ncbi.nlm.nih.gov/pubmed/18473746

Whilst the scientific community was celebrating the truly momentous discovery of a 'mixed function oxidase' another oxidase was quietly working behind the scenes, mopping up soft nucleophiles and, as it had undoubtedly being doing for aeons, aiding then unknown in the metabolism of xenobiotics and the protection of life forms. This enzyme, flavin mono-oxygenase, has subsequently been shown to be a major player, if not yet an equal partner with cytochrome(s) P450, in the metabolism of both endogenous biochemicals and foreign compounds that enter the human organism. This article outlines the importance of the flavin mono-oxygenases and examines their susceptibility to activity modulation by exogenous factors...

This would be an interesting read but sadly is not available free. It would likely make a good paper to show experts, who are likely very aware of the Cytochrome P450 group of oxidizing enzymes, but not the FMO group (which is currently recognised as being the 'trimethylaminuria causing' enzyme, but may turn out to be the 'generally smelly' enzyme, since it deals with sulfides and amines in particular).

Dr Mitchell has been responsible for many of the TMAU/FMO3 papers, and seems instrumental in instigating the first (international) TMAU workshop in 1999. It looks as if it was him who was the expert in the BBC documentary on TMAU (who the young boy visited). However he should be regarded as an FMO/TMAU expert and most of his TMAU work was done some years back. He also does work in many other areas of academic research. It's probably best to look elsewhere for expert contacts regarding fecal body odor and TMAU and other systemic body odors. Possibly those experts involved in healthcare may be more likely contacts.

Correction: the Dr in the BBC TMAU documentary was in fact Dr. Chris Hendriksz of the Birmingham Childrens Hospital

Methanogens versus the sulfate-reducers in the colon

1993: Role of dietary sulphate in the regulation of methanogenesis in the human large intestine
Christl SU, Gibson GR, Cummings JH
MRC Dunn Clinical Nutrition Centre, Cambridge

1994: Methanogens outcompete sulphate reducing bacteria for H2 in the human colon
Strocchi A, Furne J, Ellis C, Levitt MD.
Minneapolis VA Medical Center, MN 55417

It's not known if the methanogen/sulfate reducing 'war' would have any significance in a body odor problem such as fecal body odor. Some feel they can smell of rotten egg, especially after eating high sulfur food, which makes you wonder if they are obvious 'sulfate-reducer dominant' (sulfide-producing dominant) in their colon (the sulfate/sulfur being changed to hydrogen sulfide by the sulfate reducing bacteria).

The current thinking is that either methanogens or sulfate-reducing bacteria are present in the colon. People are either dominant in one or the other. They are supposedly incompatible. Both compete for available hydrogen. Two well known departments in mainstream medicine are those run by MD Levitt in Minneapolis USA, and that by Glenn Gibson in the UK (now at Reading University). Both depts seem to have come to the conclusion that both bacteria compete and that people are dominant either in one or the other.

It would be interesting if a study was ever done regarding this and fecal body odor. Perhaps all would be 'sulfate-reducing bacteria dominant', since rotten egg seems to be a common smell. Methane is seemingly odorless. A skim-read of google searches on methane suggest it may be the reason that some can do 'flame-thrower' farts (using a lighter). It is not recommended trying this at home!

Checking for methane in the 'small intestine bacteria overgrowth' breath test was added probably because of such research as above. This breath test check for hydrogen levels, but they now know that methanogens use up hydrogen too. So they wanted to make sure the lack of hydrogen was not caused by methanogens 'eating' all the hydrogen.

You would think it may be wise to add sulfide in their breath tests, since these seem to consume hydrogen as well. Sulfate reducing bacteria produce sulfide. Perhaps it may even turnout that someday methanogenic bacteria are a good probiotic, although there has been some negative research on methanogens (e.g. one paper where methanogens were associated with constipation). Currently it is not known what significance methanogens or sulfide-producing play in the colon.

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Related links:
About the small intestine hydrogen breath test

Impromptu Miami Beach Meet-Up 2009

We held an impromptu Meet-Up at Miami Beach on Saturday and Sunday, February 28 - March 1, 2009, when Glenna flew from Dallas to Tampa, Florida, and drove to Miami Beach. The same magical feeling I had experienced in the Thames Festival Meet-up crept in and possessed me all over again. The sense of retreating to a pilgrimage overcame us both.

Glenna and I spent Saturday night at South Beach where all the action was ‘til the wee hours of the morning. The night was full of music and dancing under the neon lights that adorned the art deco structures of another era. We sat at a sidewalk café with the cool ocean breeze that swayed the palm trees as the music resounded nearby and people strolled along as if not wanting to miss a thing.

My parents had been kind enough to offer us their condo on the beach, and the following morning we sat on the sand and watched the people, the boats, the jet skiers, and the birds, as we talked our hearts out. Time stood still as the hours passed, and our past, present, and our future dreams engulfed us.

We then met with Jess and Lu for an early dinner, which added yet another dimension to our meet-up. We talked for hours over good food and drinks, and none of us wanted the moment to end. We stretched it out as long as we could, but unfortunately, all good things must come to an end. Yet, the high we got from this encounter lingered for some time to come.

Here is Glenna’s version of the story. I hope you enjoy the video.







Impromptu Meet-Up in Miami By Glenna Gonzalez

It was a rush to get to Florida, with only about three days to make plans, but I got there. I was scheduled to attend a training in Tampa, Florida, but I felt heart-sick when I thought I would not be able to make it to Miami to meet Maria, Jessica, and Lucille, the only people that I know of in that area from our group. Maria is such a sweet woman that I could not fathom being any place in Florida without attempting to see her.

After completing my travel plans for the training class in Tampa, I pondered just how I could get to Miami, because I already had flight plans that led to my arrival in Tampa, not Miami. Well, the road runner that I am, I decided to drive. Driving has always been a pleasure of mine because it gives me the opportunity to clear my head and observe the scenery on those long road trips.

Here, the adventure begins. I rented a car at the Tampa airport and began my four and a half hour drive to Miami. It was nearly 6pm when I began driving, so soon there was only darkness, as I continued my trip to southern Florida. Anyway, as usual, I got lost within 15 minutes shy of Maria’s condo. This has happened to me often, in that I am usually only 10 or 15 minutes away from my destination when I somehow end up taking the wrong road (HmHm, there must be a lesson in that somewhere).

Now comes the funny part. I tried to call Maria, but the battery on my phone was low and it kept cutting off, thus I could not even finish a short conversation with her. As things would go, while driving to Miami, I had a very long conversation with my Dad. We tend to keep each other company on long drives, via our cell phones. Well, when I noticed my battery was getting low, I tried to get off the phone, but he kept going on and on. Eventually, I forgot my battery was low.

After realizing that I was lost, I pulled into the parking lot of a small strip mall. There was a cab parked there. I began to thank my lucky stars, because by now, it is nearly 12 midnight, and it is getting quite creepy (I think I was in a bad section of town). I pull up near the cabbie and he tells me that I am very far from my destination. Well, I am thinking that I either need to leave my car and catch a ride or pay him to lead me, since I think I will only get more lost. Of course, fear was setting in. By now, I have a cramp in my right leg (the one I need to push the accelerator to drive), the battery is low on my phone, I am exhausted, and some dude keeps circling me in the parking lot, like he is going to rob me or something.

Well, to my dismay, the cabbie had a very thick African accent, and was impatient as I tried to make up my mind about what I was going to do. I did talk to Maria long enough at that point to hear her say not to pay the cabbie and to try to find my way. Well, he was so mad when I told him that I would drive myself that he almost drove over my foot to leave, as I was standing near the passenger window talking to him.

So, I followed Maria’s advice. There was a car parked in front of a bank, and the driver of the car was at the ATM machine. Well, I noticed that there was a passenger in the car, so I pulled up to the right side of it to speak to the passenger, not wanting to startle the person at the ATM, for fear he might think I was going to try to rob him or something. HaHa. I pulled to the passenger’s right and began waving frantically to get his attention, and I could not figure out why he didn’t see me, when he was looking in my direction. Well, the driver walked up to me and apologized for his friend. He was blind, which is why he didn’t see me waving or trying to get his attention. I felt like a fool- one for being lost in the first place, and then second for waving at the blind passenger, who had no idea that I was even trying to get his attention. Well, anyway they gave me directions and I was on my way. They gave me excellent directions, and I was at Maria’s within 15 minutes.

I had no idea what was waiting for me. Maria was so totally hospitable and welcoming. She made me feel so comfortable. I knew that was going to be the case, because she was so excited when I called her from Dallas to let her know that I was coming to see her. We went “out on the town” of South Miami Beach until nearly 5am. We had a blast! We walked around with all the teenagers and club hoppers, taking in the beauty that is South Miami Beach during the wee hours of the morning. We went to a really cool café and had a great meal on the sidewalk, as we took in the sights. The food was totally awesome, and so was the atmosphere. Well, when we tired ourselves out, we got back to Maria’s beautiful condo, right on the beach. Maria was the perfect host and I slept so good and got up to a great breakfast.

After breakfast, we decided to hang out on the beach until we met with Jessica and Lucille. The water was the most beautiful water that I have ever seen on any beach. It was crystal clear and diamond blue. We had a great time walking on the beach, looking at the multi-million dollar condos right there, and seeing these beautiful yachts- sailing all around the area. Later, we met Jessica and Lucille at a restaurant called Flanigan’s. It was such a joy meeting Jessica, whom I have spent countless hours on the phone with, and Lucille, who has the most beautiful green eyes. We had lunch and enjoyed each other’s company, in the most spiritual way. There is nothing that I can say to explain how great that was, sitting with a group of people who could understand my deepest and utmost pain. When it was time to leave, no one wanted to. We all sat there, dreading the separation. Eventually, we did leave, but the effects of such an experience will always be with me.




Oh, how I am looking forward to the next meet-up in Miami!