A scientific paper that has just been published in journal Proceedings of the National Academy of Sciences (PNAS) examines the way that 2,4,6-trichloroanisole (TCA), the key compound responsible for musty cork taint is perceived. The results are surprising.
They suggest that TCA acts on olfactory receptor cells (the cells containing the proteins that detect smells) by suppressing protein channels called cyclic nucleotide gated (CNG) channels in the cell membranes, rather than actually eliciting odorant responses. In plain English, what this means is that we don’t actually smell TCA. These results indicate that the effect of TCA is to suppress our smell mechanism.
You can read the original paper here (it’s free to access).
This result explains why extremely low levels of TCA suppress the character of a wine, even when no musty defect is present. This is something familiar to most of us who’ve tasted lots of wines: some bottles just don’t seem right, and opening a second bottle reveals a very different wine. It’s bad news for the cork industry.
But they are also puzzling. We know very well the extremely musty smell of badly corked bottles. This paper suggests that TCA doesn’t have a smell, but that it is having its effect through suppression. The concentrations at which TCA gives a musty smell appear to be too low for activating olfactory receptors.
The authors propose two explanations. First, that the mustiness of TCA is a pseudoolfactory sensation. Second, that suppression of the olfactory receptor cell output by TCA causes an olfactory sensation.
NOTE ADDED LATER:
I have been thinking about these results. I suspect that humans actually do possess olfactory receptors that can detect TCA as a smell; these were newt cells. There is a selective advantage for humans to be able to smell TCA as it is an indicator of fungal activity. If we detect it at low concentrations and it is aversive, then this would stop us consuming food that has fungal contamination. Remember: fungi create some nasty secondary metabolites that can cause us a lot of damage. While these results explain how low levels of TCA can suppress other wine components (an observation that has always puzzled me: how would such low concentrations of one molecule affect others without such a mechanism as that explained here?), they don’t answer the question of why higher levels of TCA smell nastily musty. But even this doesn’t seem consistent: if they suppressed fruity smells, why wouldn’t they supress musty smells? It is all very intriguing, and still quite confusing.
May all the cork oaks make beautiful furniture. Lose the cork please. Such a waste of good wine when cork takes over!
The experiments were done on newt cells, and thus authors also propose this explanation for no the lack of response to YCA: “We also note that the repertoire of functional olfactory receptor genes is different between amphibians and mammals, so we cannot rule out the expression of receptors with very high TCA sensitivity in humans”
IMO there is something to be said for the experimental procedures being given more weight in scientific papers. The word “newt” is not mentioned until you get towards the end of the paper!
It is an interesting idea to explore, but it also raises a lot of questions. One of the main ones is that wouldn’t you expect something that suppresses receptors to have a lingering effect? Have you ever noticed a decline in your ability to smell good wine after tasting a TCA affected wine? I can’t say I have (not that I consider myself an expert taster in any way).
And why is it that there is a specific aromatic profile to TCA when present in high enough concentrations? We can’t all be imagining the same ‘pseudo’ smells because we were told what to expect with taint, surely?
What is intriguing, I guess, is that there is a scientific impetus to understand these issues which might make us think differently about how we appreciate wine … or maybe I’ve been reading too much wine science recently 🙂
Robert – the paper covers the “lingering” aspect. It mentions 50% recovery in 10 seconds. So unless you are doing some sort of speed tasting you should be OK with you next wine.
From a purely anecdotal point of view I have noticed the exact same thing occurring with very slightly contaminated wine. The problem is being familiar enough with the wine to know that the “muted” nose is contamination and not the wine. One more reason to buy wine by the case I guess.
It must be the season for analysing smells and how we recognise them! The BBC website reports that scientists claim that there are thousands of smells that can be categorised into just 10 basic groups.
Fragrant
Woody/resinous
Fruity (non-citrus)
Chemical
Minty/peppermint
Sweet
Popcorn
Lemon
Pungent
Decayed
Anyone with a vaguely masochistic scientific leaning can try to make sense of the journal in PLOSone.org just look for the catchily titled “Categorical Dimensions of Human Odor Descriptor Space Revealed by Non-Negative Matrix Factorization” on the home page.
It all makes for good discussion and debate. I can see where ‘gobfuls of fruit’ fits in to the matrix but what about minerality?
Just because corks have been used for generations does not necessarily mean they are still the best choice. I am wondering what the best way to seal wine would be.
they did offer an hypothesis as to why higher levels of TCA smell musty, which was pseudo-olfactory sensation.
my current studies in chiropractic have brought me into contact with a lot of cutting edge research in neuroscience, and the fact remains that the nervous system is so immensely complicated that we have hardly even begun to understand it, and how to study it effectively.
one of the things which the mind/brain/nervous system does is make things up, in the absence of other input.
to put this in different contexts, the dark and the reduced sensory input that accompanies it results in the brain doing all sorts of things which make kids really scared that there *could* be monsters or horrible things right there in the bedroom with them. not that that would ever actually be the case, but the objective reality doesn’t matter; it is the subjective experience which the mind perceives that is ‘real’, and in the lack of actual data, things get imagined. pretty consistent or similar responses in this case too, like monsters under the bed.
phantom limb pain is now understood to be the re-wiring of pathways in the brain, centrally, rather than problems with the severed nerves in the arm or leg which is “feeling” painful despite the fact that it just is not there. this explains why you can inject whatever you like into the stump of a suffering amputee with the aim of fixing the pain, and achieve no change, as that’s not where the pain is: the pain is being manufactured in the brain as it tries to figure out what this lack of input means. retraining the brain using mirror therapy and things like hypnosis and cognitive behavioural therapy, which people studying phantom pain for a long time pooh-poohed as having a placebo effect if anything at all (because those techniques didn’t look to the missing body part for the reason) are now seen as helping the brain and mind accept the lack of neural input and work around it in a fashion that is more appropriate to the function of the organism as a whole rather than trying to fill in the gaps and get it wrong.
as a chiro, the aim is to enhance or restore the function of the nervous system. there are studies underway at NZCC which show that adjusting the spine improves proprioception, which is the body’s own internal sense of where it is in space. one theory for general clumsiness and things like problems with walking or running, (repetitively sprained ankles for instance, though it need not be that overt) is that the brain (and mind, ultimately) is not receiving the proper or full information from the peripheral nervous system, and is relying on data from times gone by to send information out to make the body move. if the situation is entirely familiar then that is good enough, but what if there is something (like a divet in the grass) which is irregular? if the nervous system isn’t getting full info, and is making its response based on reduced input and ‘memory’ of the process of running, will it react quickly enough to change foot placement or muscle engagement (and prevent rolling that ankle) or will it figure it out too late (when you’re already heading for a rough landing on your knees)? bear in mind in these neural communications, things happen in the space milliseconds, so having correct, complete, timely feedback is key. the best analogy i’ve heard for this is it’s like walking down the hall to the toilet in the dark. easy to do in your own home, where you’ve done it a hundred times before, but what happens when the kids have left a whole pile of toys in the way- the good enough info that got you there the other hundred times is not going to prevent broken toys and swearing.
so coming back to the study- at a high enough concentration, it is entirely possible (especially given the near linear relationship shown between TCA concentration and nerve cells generating signals) that there is just so little info heading out of those olfactory cells to the brain, that the mind is stumped and due to there being so little input, it has to make a call on what it thinks is there. it knows what good smells are, and the way and frequency in which the olfactory cells talk when they are present, and so it decides that this lack of input is a bad smell. the sheer *lack* of signal doesn’t result in no smell, which is what common sense would say, it results in an awkward lack of neurological information, which the brain must ascribe some meaning to. and it chooses things that put you off eating or drinking whatever it is, because it knows what “good” is, and this ain’t it. why it chooses mussels and wet cardboard, i don’t know, but it was the above thinking which lead me to my twitter comment -which you may or may not recall- about that corked smell being what the brain reckons the inside of your head smells like: in the world of your nervous system, taking away all input, does not equate to the smell of “nothing” because as far as your nervous system is concerned (and smell is one of the most visceral, hard-wired of senses that is NEVER turned off no matter how unconscious all other parts may be) there is no such thing as a smell of nothing.
in fact i would go further than saying it is a “pseudo-olfactory sensation”, which implies it is a confusion of another input or sense for a certain smell, and suggest that it is a para-olfactory sensation, in that it has nothing to do with the senses themselves, and is occurring in the cortex, where inputs are deciphered and woven together, which is where we actually experience “smell”.
let me know if that just doesn’t make sense
As little as 8 molecules of a compound can trigger one human olfactory neuron. We can detect the smell of grapefruit (1-p-menthene-8-thiol) at a concentration of 0.1 ppt (0.1 ng/L).β-damascenone (fruity/exotic flowers) is detected at 0.2ppt and masks green aromas/flavours and enhances the fruity flavour perception of a wine. Compounds in low concentrations can have an impact on wine depending on the level at which we can detect it (aroma threshold). A compound can be present at a high concentration but if its threshold is high (alot of this compound is needed to smell it) it will not impact wine aroma. So if TCA is a compound with a low threshold it will probably dominate a wine.