Odor-prints: individual but genetic connections unclear

Odor is like fingerprints or facial features - it's unique.  Yet no single measurement could be easily applied to recognize an individual.

GC/MS measurements can be used to analyze mixtures of acids, alcohols, aldehydes, hydrocarbons, esters, ketones, and nitrogenous molecules in human odor. Complex algorithms mining patterns help to pinpoint the signatures. But could these signatures be easily derived from genetic makeups?

Recent article published in the Journal of Chemical Ecology looked at the usual suspects -  major histocompatibility locus (MHC) and found that these genes do not determine major patterns. 


Volatile carboxylic acids are the most diverse class of known axillary odorants, and the pattern of these acids is genetically determined. These acids  - like vast majority of human odorous compounds - are produced by human microbiome, in this case by skin bacteria. Odors of 12 families, comprising 3 to 6 siblings,were analyzed with comprehensive two-dimensional gas chromatography (GC x GC) and time-of-flight mass spectrometry (ToF MS). the analysis onfirmed the presence of individual signatures. but failed to find odors specific to HLA genes.

Even though paternally inherited HLA-associated odors were proposed to influence women odor preferences, genetic basis of odors may be more complicated than previously thought.

References

Natsch A, Kuhn F, & Tiercy JM (2010). Lack of Evidence for HLA-Linked Patterns of Odorous Carboxylic Acids Released from Glutamine Conjugates Secreted in the Human Axilla. Journal of chemical ecology PMID: 20623248

Thompson EE, Haller G, Pinto JM, Sun Y, Zelano B, Jacob S, McClintock MK, Nicolae DL, Ober C. (2010) Sequence variations at the human leukocyte antigen-linked olfactory receptor cluster do not influence female preferences for male odors. Hum Immunol. 2010 Jan;71(1):100-3. PMID: 19833159 
 
Jacob S, McClintock MK, Zelano B, Ober C (2002) Paternally inherited HLA alleles are associated with women's choice of male odor. Nature Genet 30: 175-179  PMID: 11799397  PDF
 

Foods and Smells

Image via Wikipedia

How many flavors are out there? We often hear only about these five - sweet, sour, salty, bitter and savory (umami), but there are so many more and they are important not only to our tastes but also health.

Remember that fresh grassy smell wafting up from the newly sliced tomato? It may be it's way of saying  "I'm good for you".

Stephen A. Goff and Harry J. Klee's article "Plant Volatile Compounds: Sensory Cues for Health and Nutritional Value?" published in a 2006 issue of Science explains why odors from foods may be nutritional or health signals that the human nose has learned to recognize.

Among the things emmigrants from less developed countries miss in USA is the scent of fresh tomatoes. One of the volatile compounds associated with the “grassy” tomato flavor, cis-3-Hexenal, is also an indicator of fatty acids essential to the human diet. Wild tomato contained more than three times the amount of that chemical than the cultivated version in the developed world. Two other contributors to tomato flavor — 2- and 3-methylbutanal — are indicators of the presence of essential amino acids and are also three times more common in the wild tomato. Same applies to commercial apples, strawberries, bread, cheese, even wine and beer.

Flavorful curcumin in tumeric has anti-inflammatory properties, compounds in ginger have antioxidants, and there are antimicrobial chemicals that contribute to the scent of onions, garlic, rosemary, sage, clove, mustard, chili peppers and thyme.

There are hundreds of volatile compounds in foods and beverages, often a major factor in how taste of foods is perceived.

What smells people enjoy the most?

Joanne Camas from Epicurious.com lists these 5 food smells:

1. Fried onions cooking
2. Banana bread baking (extra points if it has chocolate chips in it)
3. A perfectly ripe tomato as you slice into it, especially on a warm, sunny day
4. Coffee brewing
5. Garlic bread, fresh out of the oven
Most people commenting on this post listed baked breads and coffee as their top favorites too. Other choices include pies, spices and meats.

Here are some of the responses pulled from different blogs. What are your top five?

chefrosey 12:23:21 PM on 02/01/10

Chocolate
Fresh brewed coffee
Fresh baked bread
Fresh picked strawberries or an orange being peeled!
Any baked good coming out of the oven!

chef330 12:14:17 PM on 02/01/10

1. Onions sauteeing in butter
2. Chocolate Chip Cookies coming out of the oven
3. Just-picked peaches
4. Hot Apple Pie
5. European Butter - you can smell the flavor

Janet Tue Feb 2, 2010 2:22pm PST

apple pie baking in the oven
tralala311 Tue Feb 2, 2010 2:25pm PST

mmmm... GUMBO!!!

Habanero♥™ Tue Feb 2, 2010 2:32pm PST

Bacon, Baking Bread, Turkey, Pumpkin Pie, Molasses Cookies, Cinnamon Rolls.

Sherri Tue Feb 2, 2010 2:53pm PST

Coffee brewing, Chocolate Chip Cookies, Cinnammon Rolls, Bread, Pumkin Pie
__A_YAHOO_USER__ Wed Feb 3, 2010 9:21am PST
i think there's something about a roast that's been slow cooking all day that smells delicious, it'd be on my top 5 for sure.

Haloscan comment system closing down

 

Haloscan comment system closing down

The comment system we use for the blog, Haloscan, is closing down on the 30th December. We have exported all the comments and hope to import them into the new comment system we will use, the default system in blogger. Haloscan was never a perfect choice, but was chosen for (perceived) privacy concerns. Thank you to everyone who has posted a comment and we hope the transition to the default system goes smoothly.

Update : the blogger default comment system is now in place and seems to be functioning correctly. People can post anonymously, although all posts will be premoderated so as to avoid spam and any offence (since it's such a sensitive subject). Previously it wasn't possible to premoderate blogger comments, which is a main reason Haloscan was originally chosen.

Editor's Note (2026):

This post was originally written by blogcontributor2, one of MEBO Blog admins, in 2009, when the Haloscan commenting system was closing down. While the Haloscan name still exists in various forms today, it is no longer the same service or community platform that many blogs relied upon at the time.

Recovering this post is also a reminder of how easily knowledge disappears on the Internet. Websites close, domains change hands, commenting systems are retired, and valuable discussions quietly vanish. Patient communities are particularly vulnerable because much of their experience is shared through small websites, forums and blogs that were never archived properly.

The original MEBO website suffered a similar fate when the domain changed ownership and the blog was no longer connected, leaving years of posts effectively hidden from readers. As part of rebuilding the archive, we are restoring these articles so that the information - and the history of the TMAU community—is not lost.

Not every old idea remains current, and some scientific understanding has evolved since these posts were first published. However, preserving them provides a valuable record of how knowledge, patient experiences, and research have developed over time.

Different outcomes of TMAU urine test

 

A UK volunteer does the TMAU urine test twice and gets different outcomes

TMAU urine test results of a UK volunteer

	Jan 2009	Sep 2009	Ref. range
Urine creatinine	5.5	4.0
Trimethylamine(TMA)	56.8	32.1	2.5 - 10.9
TMA-n-Oxide	719.3	78.0	17.0 -147.0
TMA/TMA-n-Oxide	0.08	0.41	0.05-0.21

• The first sample taken in January 2009 was done with a choline food load and while directly pre-menstrual.
• The second sample taken in September 2009 was done WITHOUT a choline load and while NOT pre-menstrual.
• The tester had been following the low-choline diet between the two tests.
• The conclusions were 'secondary TMAU' in the first test, and 'primary TMAU' in the 2nd
  
• This tester is now having the gene blood test done this week. Results will be forthcoming and posted in this blog.
• Note: TMA is trimethylamine. Trimethylamine-n-oxide is the odorless metabolised end product. It is known as TMO or TMAO or TMA-n-O
  

A member of our community has kindly given permission to post her TMAU results in the blog in order to promote discussion on the current test protocol in various countries (there is no international agreed standard). These results are from the UK, and so from Sheffield Hospital, which is the only clinical tester in the UK. The parameters used were described by the tester Nigel Manning in a previous post:

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...

Nigel Manning TMAU interview

In simpler terms, Primary TMAU is a reflection of a subnormal level of conversion of TMA to TMA-n-oxide (lower than normal TMA-n-oxide production is representative of Primary TMAU). Regardless of the TMAO level, Secondary TMAU is deemed as an excessive level of TMA even if the TMA/TMAO ration is within normal limits.

In this case, while taking high choline foods, the first test shows a very high level of TMA, but her FMO3 enzyme was able to oxidize the vast majority of it, and therefore, the ratio was very low/normal. Nevertheless, the TMA present was well beyond the 'normal' range, so she was deemed as having 'Secondary TMAU' as a result.

To further confuse things, Nigel Manning mentions that he has seen cases where someone diagnosed with 'primary TMAU' (including genetic diagnosis) can later be shown to have normal levels of TMA-oxide in a later test (this should be impossible if you have genetic primary TMAU). This seems to be what is shown here. Presumably it is unknown why this is (most likely due to lack of interest from the research community)

Quote from Nigel Manning:

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.

Interestingly, in the 2nd test results where the low choline diet had been followed, the outcome diagnosis based on the 'ratio' was 'Primary and Secondary TMAU'. Her TMA level was still too high (secondary TMAU) and her TMA-oxide level was still within normal range, but according to Nigel Manning's ratio she is deemed as not converting the TMA to TMAO to a 'normal' level.

It is unclear if this particular ratio is used elsewhere. There has been mention of a different ratio used in the USA, the percentage of free TMA in regards to the whole TMA and TMAO output : TMA / TMAO + TMA.

The paper by Phillips and Shephard that is used on the NIH website describes the ratio as :

Primary TMAU parameters:

Percent of total trimethylamine (TMA) (i.e., free TMA plus the non-odorous metabolite TMA N-oxide) excreted in the urine as unmetabolized free TMA

• Severe trimethylaminuria: less than 40% of total TMA excreted as unmetabolized free TMA
• Mild trimethylaminuria: 10%-39% of total TMA excreted as unmetabolized free TMA
• Unaffected: 0%-9% of total TMA excreted as unmetabolized free TMA

NIH Trimethylaminuria explanation

It seems that whether using the percentage or Nigel Manning's ratio, both would have concluded roughly the same result here. Her percentages would have been 92.7% normal and 70.9%.

There is a pubmed paper that suggests menstruation could cause someone to be temporarily 'Primary TMAU', even if they are regarded only as a 'carrier' (of a FMO3 mutation). Perhaps the hormones have an inhibiting role on FMO3.

In comparison, three healthy control subjects that harbored heterozygous polymorphisms for [Glu158Lys; Glu308Gly] FMO3 or homozygous for wild FMO3 showed normal (> 90%) metabolic capacity, however, on days around menstruation the FMO3 metabolic capacity was decreased to ~60–70%.

Paper : Transient trimethylaminuria related to menstruation

In a citation paper done in 2008 regarding people who had been deemed 'primary TMAU' by the urine test, the citation went on to DNA test the 12 samples and only 4 were deemed 'genetically proven primary TMAU'.

In a set of our patients, two deleterious mutations were identified in 4/12 patients including a novel T237P sequence variant, while the majority of our patients (8/12) did not reveal any mutations. Some of the latter were double heterozygous for the E158K and E308G polymorphisms which could explain a mild phenotype while others had only the E158K variant which raised the question of undetected mutations. These results indicate that further experiments are needed to further delineate the full mutational spectrum of the FMO3 gene.

Genotypic spectrum and genotype-phenotype correlation of trimethylaminuria

Probably the only conclusion that can be currently made is that it is by no means a completely defined disorder and much more research is needed into trimethylaminuria. Those that can afford the test, it is perhaps best to do the urine test a few times to make sure, and the DNA test once.

Human olfactory psychophysics

 

Wednesday, June 3, 2009

Human olfactory psychophysics

This is a mainstream research paper about the sense of smell and is probably the current viewpoint of the mainstream on the olfactory system. It mentions concepts such as 'specific anosmia', 'threshold', and 'adaptation'. 'Specific anosmia' is the genetic inability to smell specific smells. Fecal body odor sufferers (or other bowel smells or other odd smells) often say they cannot smell themselves. This also seems to be the general rule for people with external body odor. However, those with fecal body odor can smell feces odor from other sources (not through human skin, it seems), so specific anosmia doesn't seem to be the reason. The same seems true for trimethylaminuria and probably other metabolic body odors, although Dr John Cashman believes that perhaps 8% cannot smell trimethylamine, although it's not known if he means only from humans or from any source. for example, most people seem to be able to smell fish. Another theory for this is 'adaptation' and desensitivity to the smell. This seems more likely than specific anosmia, however, perhaps sufferers have been in situations where a group of strangers complain of a smell but one stranger says they can't smell anything (for instance in school). Adaptation and desensitivity do not seem to account for this. At the moment it is a mystery. the most likely guess is that there is some genetic aspect, as of yet unknown.

That aside, the article is seemingly the 'latest' (2004) in olfactory perception and worth a read

Human olfactory psychophysics
Andreas Kellera and Leslie B. Vosshall 2004

Sufferer's website of body odor theories: Bodyodor777.com

 

Sufferer's website of body odor theories : Bodyodor777.com

Everybody has body odor, some more than others. This website is for those who have strong, chronic body odor and are trying to find an end to this torture. I have compiled my research in this web to help as much as possible. There is no definite remedy for everybody, but the concrete information in this web will facilitate your search to find a cure.This website, bodyodor777.com seems to be run by a sufferer trying to make sense of the maze of body odor (which as anyone with the problem knows, for the vast majority of sufferers is far more complex than society thinks). They have gathered their own ideas as to possible theories. It presents an interesting general overview of internal and external causes of strong, chronic body odor. Of particular interest is the Internal Causes section that in addition to the ones normally come to mind related to metabolic disorders, hormones, mouth, nose, throat, and intestines, it also discusses sources such as the gallbladder, kidneys, allergies, liver, food intolerance, acidic body, anorexia nervosa, and more.

http://www.bodyodor777.com/index.html

at https://www.meboblog.com/2009/01/sufferers-website-of-body-odor-theories.html 

Your gut : a bag and 2 pipes

 

Saturday, January 3, 2009

your gut : a bag and 2 pipes

stomach : small bag on the upper left abdomen. preparation bag. 

small intestine : long thin coiled pipe designed for maximum absorption
colon : wide shorter looping (one loop) pipe. recycling plant. loads of bacteria

The digestion system seems likely to play a part in fecal body odor and other metabolic body odors (e.g. secondary trimethylaminuria), so it's probably important we understand it best as possible. This post is about the basic visual and mechanical structure and main purposes. What does the gut look like and do ?

Stomach : a small bag on the upper left hand abdomen. This is where food first ends up. Generally it is held here and turned to mush and then released into the small intestine through the pyloric valve in small controlled amounts. Simple carbs won't stay long, whereas a meal will take a while. Hydrochloric acid is added to it, and some other things to make it easier to digest. The mush is called 'chyme'. Each part of the intestine is separated by valves.

Small intestine : A long thin pipe that coils in an overlapping way. This is the main absorption point. It is designed for maximum absorption of molecules of a certain small size. There are millions of finger-like microvilli on the lining (like a carpet) to make 'catching' the molecules easier. It's this microvilli that is wiped out in full-blown celiac. The pancreas puts digestive enzymes into the pipe early on to break down the food, and bile is also squirted in by the gallbladder to digest fats. The absorbed molecules go into the portal vein and then are taken to the liver for filtering before entering the main circulation. The intestine acts as a barrier so that large molecules cannot get into the portal vein unless broken down. With leaky gut (which is really leaky small intestine), large molecules can get through junctions in the barrier and so are absorbed when they shouldn't be. Because you want maximum absorption here, there is usually very few gut microbes here, especially at the top end, largely because they would compete with you for the food. The small intestine is known as 3 parts ; duodenum, jejunum, ileum. Many feel that when someone has gut candidiasis overgrowth, it's growing at the ileum (for example). However, it's likely that overgrowth of anything in the colon will cause problems too. The small intestine and colon are separated by the ileocecal valve.

Large Intestine/colon : A short, wide pipe that ascends from your appendix area, goes up to your ribcage and across, and down the other side and then loops to the anus. the colon is where most bacteria is, even in a healthy gut. Good flora scavenges from any leftover food/chyme and many produce helpful fatty acids. The protein/sulfur eating bacteria tend to be at the lower left side of the colon (near the end). The chyme becomes feces as water is absorbed and the 'rubbish' is then exited.

It's probably more complicated than that but hopefully this gives you an image in your mind of what the gut mechanically looks like.

What goes wrong ?

Some examples. If anything is wrong with the digestion enzymes such as HCL, pancreatic enzymes, bile etc, you can end up with too much undigested food entering the colon which will likely alter the flora ecology detrimentally. for instance too much protein getting into the colon.

If the tight junctions in your small intestine barrier cells are weakened you can absorb molecules too big that are not intended to be absorbed. These enter the portal vein and are sent to the liver which likely regards these as unexpected molecules.

If conditions aren't right, perhaps microbes can colonize the lower small intestine or further up.

Perhaps the colon microbes can be unnaturally altered and produce toxins. In Secondary TMAU, the diagnosis means there is too much trimethylamine produced. It's currently thought the bacteria that produce this are in the colon, so it means overgrowth of this bacteria. Who knows if this bacteria can grow in the small intestine as well. Presumably no-one is currently looking whereas a Body Odor & Research center likely would be.

at https://www.meboblog.com/2009/01/your-gut-bag-and-2-pipes.html