Why Spicy Food Burns: The Science of Capsaicin and Heat Receptors

A ghost pepper is not hot. Not in the thermal sense. You could hold one under a thermometer and it would read room temperature. Put it in your mouth and your body reports a five-alarm fire.

That gap between what’s happening and what your nervous system reports is the whole story of spicy food.

The Receptor That Gets Fooled

Your mouth, tongue, and throat contain a protein called TRPV1 — short for transient receptor potential vanilloid 1. It’s a thermoreceptor, meaning its job is to detect heat.

Under normal conditions, TRPV1 fires when it detects temperatures above about 109°F (43°C). That’s the threshold for painful heat: your body sends a signal to stop contact with whatever is burning you. It’s a protective mechanism.

Capsaicin — the active compound in hot peppers — has a shape that fits the TRPV1 receptor almost perfectly. When capsaicin molecules bind to TRPV1, they activate it at room temperature. The receptor can’t distinguish between actual heat and capsaicin. Both produce the same result: it fires and sends a signal to the brain that reads as burning pain.

Your mouth isn’t actually burning. Nothing is above 109°F. But your nervous system is receiving identical signals to what it would receive from heat that high. The sensation is entirely real. The damage isn’t.

This was confirmed in research by Caterina et al. (1997) — the team that identified and cloned the TRPV1 receptor. Their work showed that the same channel responds to both capsaicin and heat through the same mechanism. This wasn’t known before 1997. People had been eating hot peppers for thousands of years without understanding the receptor-level mechanism behind the burn.

Why Capsaicin Exists in Peppers

Capsaicin isn’t an accident. It’s an evolutionary deterrent.

Capsaicin is concentrated in the white pith (the placental tissue) around the seeds of hot peppers, not the flesh and not the seeds themselves. The plant is protecting its seeds from mammals, which chew seeds and destroy them. Birds lack functional TRPV1 receptors for capsaicin — they don’t feel the burn. Birds eat the fruit, pass the seeds intact through their digestive systems, and disperse them.

This elegant system lets peppers get seed dispersal from birds while deterring mammals. Research by Tewksbury and Nabhan (2001) confirmed this directed deterrence in wild pepper populations. The capsaicin concentration is highest in peppers growing in areas with seed-destroying mammals and lower in areas without them.

Humans adopted hot peppers and then selectively bred them for more capsaicin, defeating the plant’s entire evolutionary strategy in the process.

The Scoville Scale

Wilbur Scoville created the Scoville scale in 1912 as a measure of capsaicin concentration. The original method was genuinely unpleasant: a panel of tasters diluted a pepper extract in sugar water until they could no longer detect the heat. The dilution factor became the Scoville Heat Unit (SHU).

Modern measurement uses high-performance liquid chromatography (HPLC) to directly measure capsaicin and related compounds, then converts to SHU.

The scale isn’t linear in terms of perceived sensation. TRPV1 receptors saturate at very high capsaicin doses. Going from jalapeño to habanero doesn’t feel like going from 5,000 to 200,000 SHU in a proportional way. Your receptors max out. This is why competitive eaters can train to consume extremely hot peppers — they’re working near or past receptor saturation, not metabolizing capsaicin faster.

Why Milk Helps (and Water Doesn’t)

Capsaicin is lipophilic: it’s fat-soluble. It doesn’t dissolve readily in water.

When you drink water after eating something spicy, the water doesn’t bind to the capsaicin. It rinses the surface of your mouth and redistributes the capsaicin, sometimes spreading it to new TRPV1 receptors. The burn often intensifies briefly before subsiding.

Dairy works differently. Casein, the dominant protein in milk, is both hydrophilic and lipophilic — it has sections that attract water and sections that attract fat. This makes casein an effective detergent-like molecule. It physically binds to capsaicin and carries it away from TRPV1 receptors. This is a mechanical removal of the compound, not just dilution.

Full-fat dairy works better than skim because the fat itself also dissolves capsaicin. Coconut milk works through fat content alone. Bread works partly through physical abrasion and partly through starch binding. Beer has some fat and the carbonation may help, though it’s less effective than dairy.

The Other Spicy Compounds

Capsaicin gets all the attention, but it isn’t the only compound that produces heat sensations.

Piperine in black pepper activates TRPV1 and another receptor, TRPA1. It produces a different quality of burn — less sustained, more sharp. Black pepper’s heat fades much faster than chili pepper heat because piperine doesn’t bind TRPV1 as persistently as capsaicin.

Allyl isothiocyanate in wasabi, mustard, and horseradish activates TRPA1, which is concentrated in the nasal passages. This explains the characteristic head-clearing, sinus-opening sensation from wasabi. It’s not in the mouth the same way capsaicin is. TRPA1 in nasal tissue also causes tear production, which is why a big bite of wasabi makes your eyes water.

Gingerol in fresh ginger and shogaol in dried ginger are structurally similar to capsaicin and activate TRPV1 partially. Ginger’s warmth is milder because these compounds have lower binding affinity for the receptor.

Building Tolerance

Regular capsaicin exposure produces measurable changes in TRPV1 receptor density. The body responds to repeated activation by reducing the number of TRPV1 receptors available — a process called receptor downregulation. Existing receptors also become less responsive.

This is why spice tolerance is real. It’s not psychological, though psychology plays a role in enjoying the sensation. It’s a physical change in receptor density and sensitivity.

Tolerance is also reversible. Stop eating spicy food for several weeks and TRPV1 receptor density returns to baseline. People who grew up eating spicy food and then lived for years in a place with mild food often report losing most of their tolerance.

The endorphin connection is also real. TRPV1 activation sends a pain signal, and the body’s response to pain includes endorphin release. The rush some people describe after eating very spicy food is consistent with a mild endorphin response. For people who’ve built tolerance — who have enough receptor downregulation that the pain signal is manageable — this endorphin effect may contribute to why they enjoy hot food.