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Sunday, October 24, 2010

New paper on Asparagusuria by Monell Center

producer/excretor : produces the urine odor
perceiver/detector : can smell the urine odor
Recently the Monell Chemical Senses Center published a medical paper about the centuries old puzzlement about the odorous urine after asparagus consumption.

Asparagusuria is of interest to the body odor community, in that it seems to have similar principles to trimethylaminuria in that both seem likely due to an enzyme issue, and in both cases there seems to be a minority of population who cannot detect the odor(s) produced. In the case of TMAU, the trend seems to be that the sufferer usually cannot detect their own odor. While Asparagusuria is not reported as causing a systemic body odor, it is similar to TMAU in that both leave a compound(s) unmetabolized in the urine (i.e. TMAU leaves trimethylamine).

We have posted about the asparagusuria conundrum previously in our blog

Since Asparagusuria does not result in any known health problem, very little research has been done to discover the reasons for the phenomenom. This is also true of TMAU, even though the FMO3 enzyme has been in humans since the start of evolution and is a very commonly used enzyme by the body. Research into asparagusuria has given mixed outcomes. Probably the most in-depth research was done by Dr Steven Mitchell of London in the 1980's (who also has a TMAU research background).

non-excretors and non-detectors
The most interesting curiosities are that some people don't seem to produce an odorous urine after asparagus ingestion (non-producers) while other's do, and some seem unable to detect the odorous urine (non-perceivers). To further add to the confusion, it is not known if non-perceivers are actually non-producers and would be capable of detecting the odor in other's urine. Previous studies have again given mixed outcomes.

Is it the same enzyme problem ?
A very interesting point to this study was to find if non-producers and non-perceivers usually were genetically programmed to have both traits due to the same enzyme. This is elaborated in the quote below
The production and the perception hypotheses are often treated as if they are mutually exclusive, although there is no reason why individual differences in both production and perception cannot both be traits in the population. They might be due to the same cause. There is precedent for this hypothesis, as well: there are enzymes in human olfactory mucosa that alter molecules in ways that may change their odorant quality (Schilling 2006). Therefore, if a person lacks a key metabolic enzyme in the asparagus pathway, the inability to produce enough odorant to be detected in urine could also render the person unable to detect it (in any amount) by smell. In other words, the same enzyme could participate in both urine odorant production and in its detection. They could also coexist but be unrelated.

Because there is no known clinical problem associated with the inability to either excrete or detect the asparagus odor, the trait has received only scattered attention.
The outcome in this study did not seem to show this was the case. Of the 38 people in the study, only one had both non-excretor non-detector traits. As well as this result, the other notable results in the study were :

8% did not produce the odorous urine at detectable levels
6% could not smell obviously odorous urine
The level of odor varied

Recently a gene associated with a group of olfactory receptors was hypothesized as the receptors repsonsible for asparagusuria odor detection. This is probably what prompted this study, and it was found that there did indeed seem to be a trend to suggest this.

The inability to detect a certain odor (known as specific anosmia) is a very interesting concept to TMAU people because it is often the case that a person with TMAU and their close genetic relatives cannot smell the person. However it could also be something to do with a desensitivity to the odor. In the study, it was also suggested that inability to detect the odor was not an 'all or nothing' trait, but that detection levels varied. The various possibilities are explained in this quote :
The presumption is that one or more olfactory receptors respond to the asparagus odor but that these receptors are less functional in some people. To the best of our knowledge, there have been no family or twin studies of this anosmia, but differences in olfactory ability are due to heritable variation in olfactory receptors (Keller et al. 2007; Menashe et al. 2007), so this genetic explanation fits the available data (Eriksson et al. 2010). Although specific anosmias are often thought of as being all-or-none traits, thresholds are on a continuum and that is likely to be the case here. Some people are much less sensitive than others, but they may be able to smell the odorant if it were at higher concentrations than are usually found in human urine.

Odor sensitivity can change with repeated exposure to the odorant (Wysocki et al. 1989; Dalton et al. 2002), so someone who cannot produce the asparagus odor might be less able to smell it because they have less experience with the odor from their own urine. We cannot rule out the hypothesis that exposure to the asparagus odorant makes people more sensitive, and one limitation of this study was the lack of information about habitual asparagus intake. It is possible that genotype by experience effects might be important and that people with sensitive genotypes might become even more sensitive if they eat asparagus frequently and often produce (and smell) the odor. Future research should include the frequency of asparagus consumption to help determine the effect of experience on its perception.

Metabolites causing the odors in asparagusuria :
Surprisingly, the compounds repsonsbile for the asparaguria odor are not yet been confirmed. Previous studies have varied on suggestions for the compound(s). They all predictably think that sulfur compounds may be the culprit. A list of the previous suggestions is in the paper.

It would be interesting to know if these compounds were FMO3 substrates.

So in the end, the paper does not solve the puzzle, but it adds another group of data to the previous data published, and this time suggests the non-perception may be due to a genetic trait among a group of olfactory receptors in particular.


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