What the ...

The scene: Somewhere in Pennsylvania.

The venue: a local politician’s annual meeting with local emergency responders. Intention is to give us a pat on the back, let us listen to some interesting talks by members of our community, and generally give us the elected official’s ear for an evening.

What we were not expecting, at this gathering of largely middle-aged, white-male cops, firefighters, and EMTs, was the opening act: An interpretive dance by a young man and a young woman, to the tune of "Yankee Doodle Dandy," involving lots of saluting, leaping, and tights. Yes, tights.

Look: I don’t want to come across as some kind of Philistine here [1]. And I’m not foolish enough to think that dancers are sissies — we had one join our kendo club in Boston, back in the Before Time, and I can tell you that, within a month, he was kicking our asses with monotonous regularity. But for this audience, in this venue, it was a colossal mismatch.

We middle-aged white males have come along some, as you may have guessed from the recent election. The audience offered polite — maybe even more-than-just-polite — applause at the end. But you could also see the clockwork whirring in all the balding heads, and it went kind of like this:

What in bleeding heck was it that I just saw???

Sometimes science is like that; a new fact pops into view, and its incongruity is so striking that you literally don’t know what to do with it. But it bugs you enough that you just have to try to make sense of it.

Enter a report by Carl Philpott and crew at the universities of Leicester (I’m guessing pronounced "Lester") and East Anglia back in the Empire. This is a preliminary report of an accidental finding of superosmia — the ability to smell an odor at literally superhuman sensitivity — among a stunning 4 percent of 230 healthy subjects.

First, the background: Philpott and his colleagues were carrying out a new protocol for measuring human sensitivity, using two specific odor-carrying molecules: phenylethyl alcohol (a rose-like floral scent) and eucalyptol (three guesses). To their surprise, they found that 2 percent of healthy volunteers recruited in a hospital waiting room demonstrated sensitivity about a thousand times normal to one of the odorants when exposed to it once. When they gave another group of volunteers 10 or more trials apiece, the per-person frequency of super-smelling in at least one of the trials was a gob-stopping 10 percent. The two averaged out to just under 4 percent of all the subjects tested. Even freakier: these super-smellers sooner or later experienced a rapid loss of this hypersensitivity.

What gives? Honestly, I have no idea, and Philpott & Co. aren’t sure either. The researchers really didn’t find anything compelling on this in the past literature — the closest, a 1994 report by Amoore, even Amoore himself apparently thought was an artifact [2]. We’re all aware of the fact that many women become hypersensitive to odors during pregnancy — but the evidence suggests that’s because of a stronger reaction to odors at a "normal" level of sensitivity, not a true enhanced chemical sensitivity.

Hovering over the whole business: this is a new testing method; they might find something squirrelly about how some people test with this methodology that isn’t a bona fide sensitivity.

What biological function a random, temporary burst in sensitivity to a single odorant might have is what’s bugging me. We could be seeing something conceptually like the immune system’s random generation of antibodies with the idea that some of them will be useful for fighting infections. It’s a stretch, but it’s all I can think of.

The investigators did throw out one very neat idea for a mechanism, though. They suggested that superosmia might be “enabled by stimulation of an alternative olfactory pathway, such as the vomeronasal organ.”

Let me contextualize that a bit: The VNO is the suspected receptor organ for pheromones — airborne hormones that members of a species use to affect each others’ hormonal status, for mating, social dominance, or whatever. Its most interesting facet in this context, though, is that the receptor proteins that the VNO uses to sense pheromones are far more specific, and because of that, bind odorants far more tightly, than the olfactory receptors in the nose that detect run-of-the-mill odors.

Care to guess how much more tightly? That’s a tricky one, because the different chemical properties of olfactory (volatile) and VNO (often non-volatile) odorants make for an apples-oranges comparison. But if you guessed a thousand times — roughly the same factor as the superosmia — you’d be in the neighborhood of an admittedly crude, and maybe off-base, comparison.

In reply to some questions I emailed him, Philpott happened to mention that an earlier version of the paper, with more thoughts along these lines, ran into trouble with the reviewers. But he says that in follow-up experiments they’ll give a particularly close look to the idea that the mechanism for superosmia is the unmasking of a pheromone receptor in the human nose (which we already suspected existed).

So that’s the deal. I’m still trying to make sense of it; it feels like it ought to be important. But I still have no idea what it was I just saw. But I’m looking forward for the bigger picture to jete into view.

[1] A remarkably cultured and urbane people, the Philistines. But they picked on the wrong dudes, at least for their long-term PR.
[2] Sorry, no abstract on Oxford University Press or Google Scholar. But if you want to look up hardcopy, it’s Amoore J (1994) Chemical Senses 19:434.