On 4 October 2021 the Nobel Assembly at Karolinska Institutet in Stockholm announced that year's Nobel Prize in Physiology or Medicine. It went to two scientists, David Julius and Ardem Patapoutian, who had explained how a human being feels temperature and touch [1]. One of them had found his answer by asking a question that sounds as if it belongs in a kitchen: why does a chilli pepper burn?

The answer turned out to be bigger than chillies. It explains why ginger warms the throat on a November morning, why cinnamon glows on the tongue, why mint feels cold although it is not, and why turmeric, ginger's closest relative on the spice shelf, behaves so differently from all of them. "Warming" is not a figure of speech. As far as your nerves are concerned, it is a literal description.

This is the story of one receptor, and of the roots that learned to press on it.

A chilli in a San Francisco laboratory

Chemists had known the burning principle of the chilli for a long time. An impure extract was first drawn out of dried peppers in 1816 by Christian Friedrich Bucholz [2]; in 1876 John Thresh purified the compound and gave it the name it still carries, capsaicin [3]. In 1912 Wilbur Scoville, a pharmacist at the Parke-Davis company, gave it a ruler. He diluted pepper extract in sugar water, step by step, until most of a panel of five tasters could no longer feel the heat, and the dilution became the pepper's score [4]. The world still ranks its chillies on his scale.

What nobody knew, through all those years, was how capsaicin did it. Why should a molecule with no temperature of its own feel hot?

In the second half of the 1990s David Julius and his colleagues at the University of California, San Francisco, went looking for the answer the hard way. They built a library of millions of DNA fragments, corresponding to the genes at work in the sensory neurons that register pain, heat and touch, and put those genes one at a time into cultured cells that normally ignore capsaicin. After a laborious search, a single gene made the cells respond [1]. It coded for a channel in the membrane of the nerve cell, a pore that opens, lets charged particles rush in and fires the nerve. The paper appeared in Nature on 23 October 1997 [5].

Then came the finding that turned a curiosity about peppers into a Nobel Prize. When the team warmed the cells, the same channel opened by itself. It answers to temperatures in the range we feel as painful, from about 43 °C upwards [5]. The capsaicin receptor was a heat sensor. It was later named TRPV1 [1].

So a chilli does not resemble heat. It triggers the very sensor that tells the brain about a scalding cup, and the brain, receiving the same signal down the same nerve, reports the only thing it can: hot. It is not the only Nobel Prize hiding in a plant, either; beetroot has one of its own.

A sensor that adds things up

A year later the same laboratory showed something worth remembering whenever a recipe pairs ginger with lemon and hot water. Acid lowers the temperature at which the channel opens: in mildly acidic conditions, at pH 5.9 or below, it fires at room temperature. The authors called the receptor a molecular integrator of the chemical and physical stimuli that we feel as pain [6]. In plain words, it adds its inputs together. A little heat, a little acid and a little of a pungent molecule each bring it closer to opening.

Ginger carries the same key

Capsaicin belongs to a chemical family called the vanilloids, after a small ring-shaped group of atoms it shares with vanillin, the molecule that gives vanilla its scent. That group is the head of the capsaicin molecule, the part that settles into the receptor [11]. Ginger's pungent compounds, the gingerols, carry the same group [12].

In 2002 a team at the University of Sydney tested them directly on sensory neurons. 6-gingerol and 8-gingerol produced the same calcium surges and electrical currents as capsaicin, and a drug that blocks the capsaicin receptor shut the response off. They gave the paper a title that says it all: "Gingerols: a novel class of vanilloid receptor agonists" [13]. Ginger, in other words, is not merely like chilli. On the nerve it does the same thing through the same door, only more gently.

What happens next depends on what you do to the root. Fresh ginger is rich in gingerols. Dry it or heat it and the gingerols lose a molecule of water and become shogaols. Measured per gram of dry matter, fresh rhizome holds about 5.9 mg of 6-gingerol and less than 0.1 mg of 6-shogaol, while dried ginger can hold up to 3.7 mg of 6-shogaol [14]; the conversion is strongest with hot-air drying at 150 °C [15]. And when researchers in Japan put the whole series to the receptor, every gingerol and every shogaol activated TRPV1, the shogaols more strongly [16]. That is why powdered ginger bites differently from the fresh root, and why a cold-pressed juice of fresh ginger keeps the rounder, greener warmth of the gingerols.

Ginger is also the one plant on our shelves whose rhizome the European Medicines Agency has granted well-established use status, its highest herbal category, for preventing the nausea of motion sickness [17]. What it does in the season of sore throats we have set out in The First Cold of the Season. It is the root we press almost neat for Root Boost, and the reason ginger runs through four of the five shots in our Shield line.

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Turmeric, the quiet cousin

Turmeric and ginger are family in the botanical sense: both belong to the Zingiberaceae [18], and a fresh turmeric rhizome looks like a small ginger root until you cut it and find it orange. The colour is curcumin, and curcumin's history is as long as capsaicin's. It was first isolated from turmeric in 1815, one year before Bucholz drew his burning extract out of chilli peppers [19].

For most of the two centuries since, chemists valued curcumin as a colour. It turns from yellow to red when a solution becomes alkaline, and it still appears on food labels as the colour E 100 [19][20]. Even the English name is a puzzle about colour and earth: "turmeric" has been compared with the medieval Latin terra merita, "worthy earth", and may equally be a garbling of the Arabic kurkum, a word that covered both this root and saffron [10].

Now look at the molecule. Curcumin is built from two of the same vanilloid rings that capsaicin and the gingerols carry, joined by a short chain [19][21]. On paper it ought to be the hottest of the three. It is not hot at all, and the receptor explains why. Curcumin does not open the chilli channel. In experiments in Seoul it did the opposite: it damped the current that capsaicin switches on, and in rats it blocked the heat sensitivity that capsaicin causes [21]. What curcumin does open is a second channel, TRPA1, which it first activates and then quietens [22].

So the two cousins divide the work. Ginger presses the heat sensor. Turmeric leaves it alone and brings other things to the bottle: the colour, an earthy bitterness, and an aromatic oil that the fresh rhizome keeps and the dried spice largely loses. In fresh turmeric about 60% of that oil is turmerone; in the dried rhizome the figure falls below 7% [18]. That is the case for pressing turmeric fresh, as we do for Golden Blend, where it sits beside ginger, apple and lemon.

One more piece of curcumin chemistry is worth knowing before you pour. It breaks down quickly in sunlight, which is why a turmeric stain fades fastest on the washing line, and why turmeric juice belongs in the fridge door and not on the windowsill [19].

Cinnamon, mustard and the other half of the prize

TRPA1 has a story of its own, and it leads to the second laureate. In 2004 Ardem Patapoutian's laboratory showed that this channel is activated by the pungent compounds in cinnamon oil, clove oil, mustard oil and ginger, and that cinnamaldehyde, the molecule that makes cinnamon taste of cinnamon, is its most specific activator [23]. In the same year Julius's group showed that mustard, horseradish and wasabi work through the very same channel, on nerve fibres that also answer to capsaicin [24].

That gives the spice shelf a simple map. Chilli and ginger open TRPV1, the heat channel. Cinnamon, mustard and, more quietly, the curcumin of turmeric open TRPA1, its neighbour on the same nerve endings; ginger has a foot in both camps [23]. A blend that carries ginger, turmeric, chilli and cinnamon together, as Crimson Ember does, is therefore not four versions of one sensation. It is a chord: two receptors and four kinds of molecule, each with a character of its own. Berry Blaze is the single note, aronia and chilli with nothing between you and the capsaicin.

Does the body actually get warmer?

Feeling warm and being warm are not the same thing, so it is fair to ask whether anything measurable follows once the nerve has fired. It does, and the route is known. In rats, gingerols and shogaols raised the secretion of adrenaline from the adrenal glands, and for the shogaol the researchers tested, blocking TRPV1 stopped it [16]. The receptor is wired to the hormone that turns the body's burners up.

In people the effect is modest and real. At Columbia University ten overweight men ate the same breakfast twice, once with 2 g of ginger powder dissolved in hot water. With ginger, the energy they spent digesting the meal rose by about 43 kcal a day, and they reported less hunger [25]. In Japan six women with cold-sensitive hands and feet drank 280 ml of a ginger beverage or a placebo in a room held at 21 °C, while a thermal camera watched their palms. Both drinks warmed the hands at first. After the placebo the temperature fell back within 10 minutes; after ginger it went on rising for 20 minutes and stayed up significantly longer [26].

The chilli side of the family tells the same story. A meta-analysis of the human trials concluded that capsaicin raises energy expenditure and fat oxidation, by a small margin [27]. When 18 young men swallowed capsinoids, the non-pungent relatives of capsaicin, energy expenditure rose only in those who had active brown fat, the tissue that turns fuel directly into heat [28]. An extract of grains of paradise, a member of the ginger family that carries 6-gingerol and 6-shogaol, did the same in a study of 19 men [29].

None of this makes a ginger shot a diet, and we would not sell it as one. What the numbers show is that the warmth is not imagined. A pungent root on the tongue is followed by a body that makes a little more heat. On a dark morning at our latitude, where the sun sets before four for more than six weeks of the year, that is exactly the feeling people have reached for ginger to get for as long as ginger has been traded.

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From the laboratory bench to the kitchen shelf

Everything above fits into three small habits.

Keep it fresh

Gingerols belong to the fresh root and turmerone to the fresh rhizome; drying changes both [14][18]. A cold-pressed shot is the fresh profile in concentrated form. Wild Kick is the plainest way to taste it: 90% aronia, 10% ginger and nothing else.

Try it warm

The receptor adds heat, acid and pungency together [6]. Stir a shot into a cup of warm water, not boiling, and notice what the same 60 ml does: you are handing the receptor two of its signals at once. A shot that already carries lemon hands it the third.

Give it company

The ginger in the Columbia study was taken with breakfast [25]. A shot beside the first meal of the day borrows the timing of that study, and it is the easiest habit to keep.

One caution. Concentrated ginger and turmeric are food, but they are strong food. If you take blood-thinning medicine or are pregnant, ask your doctor or pharmacist before you make them a daily habit [30].

In 1997 the question was why a chilli burns. The answer was a single protein in the membrane of a nerve, one that cannot tell a hot stove from a hot pepper and was never built to. Plants found it long before we did. Ginger learned to press on it, and cinnamon and turmeric on the one beside it. People have been glad of the result for a very long time without knowing the reason. Now we know the reason, and it is still a good idea.

References

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19. Priyadarsini KI. The chemistry of curcumin: from extraction to therapeutic agent. Molecules. 2014;19(12):20091–20112. doi:10.3390/molecules191220091
20. EFSA Panel on Food Additives and Nutrient Sources added to Food. Scientific opinion on the re-evaluation of curcumin (E 100) as a food additive. EFSA Journal. 2010;8(9):1679. doi:10.2903/j.efsa.2010.1679
21. Yeon KY, Kim SA, Kim YH, Lee MK, Ahn DK, Kim HJ, Kim JS, Jung SJ, Oh SB. Curcumin produces an antihyperalgesic effect via antagonism of TRPV1. Journal of Dental Research. 2010;89(2):170–174. doi:10.1177/0022034509356169
22. Leamy AW, Shukla P, McAlexander MA, Carr MJ, Ghatta S. Curcumin ((E,E)-1,7-bis(4-hydroxy-3-methoxyphenyl)-1,6-heptadiene-3,5-dione) activates and desensitizes the nociceptor ion channel TRPA1. Neuroscience Letters. 2011;503(3):157–162. doi:10.1016/j.neulet.2011.07.054
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This article is for educational purposes and is not medical advice. If you have a diagnosed condition, are pregnant or take regular medication, speak with your doctor or pharmacist before changing what you eat or drink.