The mysteries of chili heat: Why people love the pain
When eating hot peppers the difference between “just right” and “ouch” is razor-thin. Here's why
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Chili heat is painful, yet enjoyable; fiery, with no rise in temperature. In 1953, T. S. Lee, a biologist at the National University of Singapore, tried to unravel the physiology behind this reaction. He asked a group of forty-six young men to eat chilies, and monitored their sweating. Perspiration is a physiological reaction to heat. Rising body temperature, whether from the surroundings or from muscles warming during exercise, triggers a reaction in the hypothalamus. Via a series of feedbacks between the brain and the body, sweat glands go to work. Sweat evaporating off the skin cools the body; when its temperature drops back to normal, it stops.
Lee had the volunteers dress in cotton trousers only, then painted their faces, ears, necks, and upper bodies with a solution of iodine and dusted them with dry cornstarch—a combination that makes sweat turn blue. Lee used peppers common in Asian cuisine, from the species Capsicum annuum. Their tapered red fruits are about ten to twenty times hotter than jalapenos. For the sake of comparison, at a different time Lee’s subjects also taste-tested solutions of cane sugar, bitter quinine, acetic acid, potassium alum (an astringent that makes the lips pucker), ground black pepper, mustard paste, and hot oatmeal. Some also gargled with hot water, chewed rubber, or swallowed feeding tubes.
In one experimental run, after eating chilies for five minutes straight, the subjects flushed red in the face, then all but one began to sweat. The areas around their noses and mouths turned blue, followed by their cheeks. Lee did another trial with seven participants, feeding them one pepper, then another: five continued to sweat, two profusely. Among the controls, only the acid and ground pepper made the volunteers sweat.
Eating chilies doesn’t raise body temperature, so there is no physical need for cooling. Yet in Lee’s experiment, the subjects sweated as if they had run a mile on a hot afternoon. To verify that the reactions to chili heat and genuine heat were equivalent, Lee had some volunteers put their legs in hot water. As their temperatures rose, the patterns of sweating on their faces were identical to those produced by eating peppers. Lee had already deduced that chili heat could not be a taste, because people felt its burn on their lips, where there are no taste receptors. His experimental results indicated another body system was at work: the one that registers discomfort from burning. The chili burn was a form of pain. But it differs in one important respect: touch boiling water, and the pain intensifies until the hand is withdrawn. Start eating a Carolina Reaper, and the heat builds for several minutes, becoming overwhelming. But continue, and the heat recedes, leaving the mouth numb to chili’s effects. Capsaicin causes pain, then blocks it.
Chili extracts have been used as painkillers for centuries or longer, stretching back into the pre-Columbian era. In 1552, a pair of Mexican natives, Martín de la Cruz, a healer, and Juan Badiano, a teacher, collaborated on a guide to Aztec herbal remedies now known as the Badiano Codex. It makes extensive use of the analgesic properties of chilies. One remedy for inflamed gums was to make a compress: boil the roots of several kinds of pepper plants along with a chili paste, wrap the resulting stew in cotton, and press it against the afflicted
area. Elsewhere, native Americans rubbed hot peppers on their genitals to dull sensation and prolong their sexual pleasure—something early Spanish settlers also tried, to the dismay of prudish priests accompanying them. In nineteenth-century China, chili extracts were used as a local anesthetic for men about to be castrated to serve the emperor’s court as eunuchs. It was capsaicin’s painkilling potential that the chemist Wilbur Scoville was trying to exploit when he developed his eponymous heat scale a century ago. He worked at the laboratory of one of the world’s leading drug manufacturers, the Parke-Davis Company, outside Detroit. Parke-Davis and other pharmaceutical makers of the era were finding new ways to use plant alkaloids, including capsaicin and cocaine. (Parke-Davis once paid Sigmund Freud twenty-four dollars to rate its cocaine products, including a powder and an elixir, against those of its more established German rival, Merck. He noted only a small difference in taste, writing: “This is a beautiful white powder (available at a low price).”
Capsaicin was the active ingredient in Heet Liniment, Parke-Davis’s topical painkiller cream. Scoville was assigned to measure the relative hotness of various pepper plants and concentrations of capsaicin, so that the correct dose could be more accurately gauged. Too much capsaicin burned unpleasantly; too little didn’t work. Capsaicin had been isolated in 1846 by John Clough Thresh, who named it, and also noted that it was chemically related to vanilla. Capsaicin and its relatives, the most pungent compounds in the world, are molecular cousins to one of the gentlest, smoothest flavors. In 1912, there was no simple chemical test to detect capsaicin—only the sense of taste. Scoville ground up dried peppers and prepared extracts of different strengths. He assembled a panel of five lab colleagues. If a sample tasted hot, he diluted it repeatedly until no heat could be detected. The more dilution required to eliminate the last trace of burn, the hotter the pepper was.
Scoville had found a way to quantify a subjective sensation, an important achievement. He called it the Scoville Organoleptic Test, with heat measured in Scoville units. A rating of one million Scoville units meant that the extract had to be diluted to a concentration of one part per million before its heat disappeared. This approach was somewhat imprecise, because people have varying sensitivities to heat just as they do to other flavors, which is why today, the absolute concentration of capsaicin in a pepper is measured with a chromatograph and then converted to Scoville units.
Parke-Davis never succeeded in making capsaicin into an effective, profitable product. Heet is still sold today and still contains capsaicin, but the primary active ingredient is now methyl salicylate, derived from wintergreen. Today, five centuries after the Badiano Codex and one century after Scoville, drug companies are still trying to exploit capsaicin’s numbing effect with dermal patches, injections, and other approaches, but success has largely eluded them. Manipulating the body’s heat-sensing system is a dangerous business; in tests of one of these pain blockers, animals developed persistent high fevers: their bodies literally overheated. Drug companies and biologists of Scoville’s era who studied capsaicin’s peculiar effects encountered the same obstacles that hampered the understanding of taste. They knew some kind of biological alchemy was occurring among capsaicin, body, and brain, but couldn’t pinpoint how it worked. Decades later, the key to this mystery was found in the milky sap of the resin spurge, a cactus-like plant that grows in the Atlas Mountains of Morocco. Moroccans slash open the plant, let the sap run out and dry, and harvest and sell the resulting resin, which contains the most powerful chemical irritant known: resiniferatoxin, or RTX for short, a form of supercapsaicin. Pure capsaicin rates at 16 million Scoville units; RTX rates at 16 billion, a thousand times hotter. Touching resin spurge sap causes severe chemical burns; swallowing more than an eyedropper full is fatal. Yet when greatly diluted, it has powerful medicinal qualities. In the first century AD, Juba, a North African king who was married to a daughter of Marc Antony and Cleopatra, had a terrible case of constipation, and his Greek physician Euphorbus prescribed some sap that had been dried, ground up, and cut with water. (The word “spurge” derives from the French word for “purge.”) This ancient laxative worked so well that Juba named the plant “Euphorbia,” after his doctor. Centuries later, Carl Linnaeus followed suit and named this genus of plants Euphorbia, and this particular one Euphorbia resinifera. Today, the resin is used to treat nasal blockages, snakebites, and poisons.
In the 1980s, RTX caught the attention of scientists studying the chili burn. Since it was so much more powerful than capsaicin, even the tiniest amounts made tissues flare in response. Research accelerated. When applied to the skin or injected, scientists found that RTX tricked the brain and body into thinking that room temperature was hotter than brimstone; then it abruptly shut down the body’s ability to sense heat, or respond to any temperature changes. Rats treated with RTX developed hypothermia. But unlike a topical anesthetic, which numbs all feeling, RTX did not impair other kinds of touch; the rats could still feel a pinch or an electric shock. Only nerves that sensed heat were affected. In one experiment, scientists irradiated a bit of RTX to make it traceable by scanner, injected it into a cell, and observed as its molecules attached themselves to a previously unknown kind of receptor: a heat receptor.
Lee’s sweat-while-you-eat experiment from forty years earlier had been vindicated. Both RTX and capsaicin molecules attached themselves to the body’s receptors for registering heat and pain. These are part of a larger family of sensors that detect grave threats: heat, cold, burns, blows, cuts, pinches, electrical shocks. Without them, humans would die rather quickly.
Capsaicin receptors are embedded in the surface of nerve cells in the mouth, skin, eyes, ears, and nose. When these cells come in contact with anything hotter than 108 degrees Fahrenheit—the signal that the line between “toasty” and “too hot” has been crossed—the receptors’ shape changes in response. This opens a pore to the cell’s interior. The water in the human body is a salty soup of positively and negatively charged particles, diffusing in and out of cells. The pore is only one or two atoms wide, and allows only positively charged calcium ions through. The electrical charge makes the neuron fire, sending a signal to the brain. This process takes only milliseconds, a much faster reaction time than that of taste receptors. Thus the hand jerks away from a hot pan before awareness catches up.
Chilies trick this system. Begin eating a hot pepper, and capsaicin molecules inundate these receptors. This lowers the mouth’s heat threshold, much as salt lowers the melting point of ice; suddenly 98.6 degrees feels like 150. This is why chili peppers taste hot. The heat alarm reaches the brain via the trigeminal nerve, one of the major neural pathways in the head, relaying signals from the face, the nose and mouth, and the eye. The chili burn is the strongest of a number of “tastes” sensed by receptors for heat or touch and carried by the trigeminal nerve that include the sharp pungency of horseradish and wasabi, the gentler tang of lemongrass, and the hot tingle produced by the Szechuan pepper (which is not related to chili or black pepper). Szechuan peppers are also used as an ingredient in lipsticks to inflame the skin and simulate the sensation of pouty lips.
So, pain is a distinct part of flavor, with its own unusual properties. Heat receptors are present all over the body, which makes superhot chilies dangerous. An unpleasant taste can only be sensed by the tongue, but capsaicin envelops you, as my son and I found while watching Ed Currie prepare hot sauce. He poured a bottle of white Bhut Jolokia pepper mash—a beige-colored, six-to-one mix of pureed pepper and vinegar—into a pan, blended in additional spice, then put the mix on the stove. Capsaicin in the steam stung our eyes, then reached our noses, and we coughed and sneezed for ten minutes. Currie appeared immune.