When I first met Zack, I expected to get a lot of things from him--companionship, friendship, company when I went out jogging. What I didn’t expect to get was fleas. Nevertheless, it was Zack who gave me my first--and mercifully only--case of insect infestation, and even 15 years later I still find it hard to forgive him.
Zack, I should hasten to mention, was not a friend, nor a family member, nor a college roommate (though a number of people in this last group did turn out to be generous sources of fleas themselves--especially the ones who spent most of their waking hours learning to play Layla in really bad bands). What Zack was, was an Irish setter, the bison-size pet of a friend with whom I shared a house in graduate school. Zack’s full name, according to his pedigree papers, was Zachariah of Sutherland, but I knew him better as Zachariah of Large Clumps of Red Fur Stuck to Every Piece of Furniture in the House. Zack’s biggest problem wasn’t that he shed (though he did, usually at a rate of about one cardigan sweater and a pair of matching mittens’ worth a day). Nor was his biggest problem that he was a tad, well, frisky--a perfectly fine trait if you’re a kitten or a puppy, but not so fine if you’re a full-grown hunting dog with all the grace and light-footedness of a Pontiac minivan.
No, Zack’s biggest problem was that he had fleas. And not just a few fleas, mind you; not even a garden variety lot of fleas. Zack, as near as I could tell, had all the fleas. For a brief period in the 1970s, pet owners around the world began reporting that their dogs’ fleas were packing up, jumping ship, and running away to go live on Zack. I never knew where Zack picked up his first fleas, but I did know where he left them: in a fossilized shag carpet in my bedroom.
The first clue I had that there were bugs in my Olduvai rug came one night when I awoke to find that I was itching maddeningly. Throwing off the sheets, I discovered that my legs were covered with more bites than I could count, that I was scratching compulsively in much the same way Zack was, and that I had a sudden urge to growl at the mailman and drink out of the toilet. The answer, of course, had to be fleas, especially since my bites were only from the knees down. Unlike most insect pests, fleas can’t fly, but they can jump--covering the distance from the average floor to the average knees in a single boing. At flea scale, that’s like doing the World Trade Towers in socks.
I spent much of the rest of the night in something approximating itch agony, clawing at my suffering limbs, covering myself with enough Lanacane cream to swim the English Channel, and, in lucid moments, wondering just what it was that was responsible for this excruciating, sleep-robbing sensation. Why do we experience itching? What possible survival value can it have? And is it possible to kill an Irish setter and dispose of the body without the owner noticing?
As it turns out, at least the first two questions have been asked by people other than just me. Indeed, the itching phenomenon, from poison ivy to mosquito bites to tinea cruris (also known as jock itch, or that disorder that guarantees you your own seat on the locker-room bench), has been a long-standing mystery to science. Now, however, answers may be on the way. With the help of a new understanding of nerve fibers, skin receptors, and pharmacology, investigators are at last beginning to solve one of the body’s most enduring and least endearing puzzles.
The latest salvo in the itch wars was fired last April when Malcolm Greaves, a dermatologist at the St. John’s Institute of Dermatology in London, wrote a broadside on the topic in the New England Journal of Medicine. The paper started off promisingly enough, running under what for the New England Journal was the near-madcap title of Itching--Research Has Barely Scratched the Surface. Soon enough, however, the Journal lapsed into more-familiar doctor-speak, chattering on about polymodal nociceptors, dorsal horn cells, and fast-conducting afferent nerves and even replacing the reader-friendly term itch with its swaggering synonym pruritus. Obviously I had to get hold of Greaves himself to help me sort through some of the jargon. The problem was that the prospect of tracking down the doctor in his UK lab made me a little nervous. A hopeless frontier yahoo, I’ve always been a bit intimidated by the ability of the average English man to make the average American man feel like the average Piltdown man.
When I got Greaves on the phone, things were even worse than I’d imagined. He acknowledged that yes, he had written the paper, but no, he didn’t want to talk about it--at least not to me. (Perhaps he had heard as much about my work as I had about his.) Suppressing an urge to remind him that swapping high-level pruritus intelligence was not exactly the stuff of Senate espionage hearings, I asked him instead if he might have five minutes to share at least a bit of his itch wisdom--like just what is an itch? Is it simply a subtler form of pain, or is it a whole different breed of neural mischief? With a deep, scepter’d sigh, Greaves responded.
The itch sensation, Greaves explained, is carried by very thin sensory fibers that are dedicated either to transmitting itching or to transmitting pain. Experiments tell us that there are nerves set aside to carry one sensation or the other but not both.
The experiments Greaves referred to involved first rounding up groups of courageous volunteers and inserting needle-sharp electrodes into their ulnar nerves, or funny bones. The funny bone, of course, with its singular ability to reduce even the strongest person to a small puddle of Smucker’s, is one of the body’s zaniest pranksters, close kin to merry migraine and rib-tickling kidney stone. Once the itch researchers had their ulnar electrodes in place, they threw a switch sending a low-level current through the needles and then sent highly trained technicians into the lab to scrape the volunteers off the ceiling with a putty knife.
Actually, the currents used in the studies were not enough to lead to any real pain; the volunteers merely experienced a range of sensations from an itchy tickle to an achy twinge. Intriguingly, when the currents were low enough to cause just an itch, they appeared to stimulate one set of fibers in the ulnar nerve; when they caused pain, they stimulated another.
Nerve fibers, it turned out, are just like different electrical cables in a house, Greaves said. Structurally, they’re all exactly the same and could carry any type of current, but some are assigned to carry only AC, and some are assigned to carry only DC.
For me, the studies raised almost as many questions as they answered, and I was eager to learn more. Unfortunately, it was at this point that Greaves decided he had said all he intended to and left the phone to hide whatever else he knew about itching inside a hollow pumpkin in the hope that Whittaker Chambers might show up. For further help, I had to turn to another itch engineer, Jeffrey Bernhard, director of the dermatology division at the University of Massachusetts Medical Center.
Itching is not just a subtler form of pain, Bernhard said, though in some cases the intensity of the stimulus is enough to determine whether we’ll feel pain or whether we’ll feel an itch. In other cases, however, intensity has nothing to do with it. Morphine, for example, is a drug that has the power to relieve pain but can actually cause itching. Here it is chemistry that determines which sensation will be felt.
But what is the purpose of feeling an itch at all? Apart from dogs, cats, and the occasional N.F.L. fan, no one actually looks comfortable lying around scratching, so why on earth do we do it? Itching is an adaptive trait, Bernhard said. It arises because the body believes that some noxious substance or pest has intruded onto--or into--the skin. Scratching is an attempt not only to ease the uncomfortable sensation but to dislodge the pest.
Among the unwelcome invaders our bodies try to shake loose by scratching are mites, which irritate itch receptors when they burrow into the skin; lice, whose saliva contains an anticoagulant that helps them dilute and drink our blood but that also triggers an allergic itch reaction; fleas and mosquitoes, whose nips are equally noxious but who usually manage to be long gone before we get around to scratching; and fungi, like athlete’s foot or jock itch, which take root in the skin and cause inflammation that leads to itching. Though scratching is ineffective against some of these invaders--especially fungus--the body doesn’t know that. It only knows that the skin has been irritated or assaulted and that a scratch seems to be called for. (Incidentally, though most victims don’t know it, the tinea cruris [jock itch] fungus is almost identical to the tinea pedis [athlete’s foot] fungus, with the exception that the cruris variety got an even worse place to live. Some pharmaceutical companies take advantage of this ignorance by marketing athlete’s foot and jock itch products separately, when one might take care of both problems. This information came as a boon to a person I know--let’s call him me--who was always too mortified to buy any product with the words jock and fungus appearing on the same label. Of course, as any fungal support group will tell you, jock itch is absolutely nothing to be ashamed of, and indeed, some of the immortals of sport were thought to suffer from the problem, including Stan The Man Musial, Babe The Sultan of Swat Ruth, and Darryl Nobody Asks to Borrow His Towel Strawberry.)
Though scratching might not always be effective in freeing the skin of an itch-inducing agent, there is no question that it temporarily frees the host of discomfort. But just how it does this is unclear. The most obvious answer is that the relatively subtle itching sensation is no match for a vigorous scratching session, and the second stimulus simply swamps the first. Some researchers, however, propose much more elegant answers. One hypothesis holds that scratching anesthetizes a nerve by temporarily deactivating it. A nerve may have several receptors, each of which can be stimulated only a certain number of times before it becomes exhausted and has to be replaced by a fresh one. Scratching, it is thought, accelerates this burnout process, exciting receptors to the point that they overload.
Just as important as neurology in the itch-and-scratch cycle, however, is psychology. Itching is a little like breathing, said Bernhard. You’re fine until you think about it, then you can’t get it out of your head. Anyone with a pruritus problem will tell you that their itching is at its worst when they have nothing to distract them.
Bernhard’s observations are certainly borne out by my own itch experiences. One July, while away at summer camp, I was walking through the woods when I stumbled upon an outcropping of poison ivy larger than most island nations. By the time I got back to my bunk, I had already begun to swell into something resembling a four-and-a-half-foot Michelin man, only not as svelte. For the next several days my itching so consumed me that I was unable to participate in any camp activities--including making fun of Lenny Weiner during afternoon rest period, a camp-wide pastime so popular it had become an official part of the summer curriculum. The only thing that took my mind off my suffering occurred several nights later when Mark Friedman--a leading wit in 1965, provided you were male and under 11-- entertained the bunk during dinner by putting French dressing in his hair while singing the lyrics to the Dippity-Do commercial.
Of course, the majority of us will not always have Mark Friedman and a pint of salad dressing handy, so for lasting itch relief, we must sometimes turn to Combe, Inc., of White Plains, New York, one of the nation’s leading manufacturers of anti-pruritus products. For years Combe has produced a range of innovative goods vital to keeping America competitive in a twentieth-century global economy--including Odor-Eaters, a product that goes a long way toward proving that Yankee ingenuity can still beat the pants off the Japanese in the cutthroat smell-absorbing shoe-liner market, and Just For Men hair coloring, a grooming breakthrough that gives average guys like you, me, and former president Reagan the opportunity to have a full head of lush, dark hair that looks exactly as if it were assembled from 10,000 fresh licorice whips.
Leading Combe’s merchandise list, however, is its arsenal of itch medications, including Lanacane, intended to treat ordinary, epidermal itching; Lanacort, intended to treat itching accompanied by inflammation; and Vagisil, intended to treat, uh . . . poison ivy. Yeah, that’s it! Poison ivy! Behind all of these products is Combe ointment czar Herbert Lapidus, a pharmacologist who has been with the company for 22 years and has invented some of its most successful products. It was Lapidus who helped develop topical creams that could--in the words of the irrepressible imps in Combe marketing--shut off the itch like a switch.
One of the earliest itch researchers was a Dr. J. Adriani, from New Orleans, Lapidus says. He was the first to show that various concentrations of anesthetics like benzocaine, lidocaine, dibucaine, and tetracaine could be effective against topical itching. Adriani’s work, of course, wasn’t wholly new; the similarly surnamed medications he studied were all members of a family of compounds that also includes the common dental anesthetic novocaine. The difference is that unlike novocaine--which must be administered subcutaneously with needles slightly larger than the Eiffel Tower--the other caine kin are able to work on the surface of the skin.
Nobody is entirely certain how topical anesthetics work, says Lapidus, but it’s generally believed that there’s a threshold of sensation that must be crossed for a nerve ending to react, and what the anesthetic does is raise that threshold. Mixed with a cream that also cools and moisturizes the skin, the anesthetic can break the cycle of scratching that leads to more itching that leads to more scratching that leads to more itching. In these cases, Lapidus explains, the body essentially works against its own best interests, continually signaling us to defend an irritated patch of skin by scratching it, even though that only makes the problem worse. But why would we develop such a half-baked response? Where’s the evolutionary logic in that?
Just because scratching is an adaptive trait, Lapidus says, doesn’t mean it works perfectly.
Lapidus could easily have gone on in this vein for much of the day. But after Lanacane, I knew, would come Vagisil, and after Vagisil we’d be only a stone’s throw from a competing company’s Anusol--and I wanted no part of that. For the most part, my itch for knowledge had been scratched, and I saw no need to have Lapidus stimulate my receptors further.
Of course, just because I had heard all I needed to did not mean that there aren’t countless pruritus puzzles yet to be solved. For instance, why is it that your foot never itches when you’re wearing just a pair of socks but drives you mad the second you put on a pair of ski boots with more snaps and fasteners than a lunar suit? Why isn’t there some way to scratch a tickle in the back of your throat without making a noise that sounds like you’re about to produce a loogie the size of a love seat? How did they come up with the name Anusol anyway, and did somebody fire the focus group?
These are all good questions, I think, and someone should answer them. However, I’m definitely not the guy. Having spent the better part of a month prattling about pruritus--and scratching everything but my incisors--I have had enough itch talk to last me until I’m 90. Or at least until I meet my next Irish setter.