It’s hard to imagine how taste can affect our pain. Why should it matter if something is salty, sweet, spicy, or bitter? Yet more and more studies are showing how taste and pain are intertwined.
Sugar is routinely used to comfort neonates undergoing painful procedures. And in one study the subjective perception of pain intensity and unpleasantness was reduced in adults when given sweets over bitter tasting foods. We’ve all experienced this phenomenon when we seek out comfort foods. Even hot and spicy foods appear to alter pain centers in the brain.
We each have between 5,000 and 10,000 taste buds in the back of the mouth and on the palate. Each taste bud consists of 50-100 specialized cells called papillae which are stimulated by taste e.g. sugar, salt, acids. And up to three quarters of those sensory receptors in the papillae have nerve fibers wrapped around them that sense temperature, touch and pain. They couldn’t be physically closer! When these nerve fibers are activated, signals are sent to the thalamus which then forwards them to specific areas in the cerebral cortex giving us our sense of taste. That means the neural circuitry the brain uses to categorizes taste, temperature and pain-related sensations all lie in a common area which then defines these sensations as either pleasant or unpleasant.
In the past, we were taught that different areas of the tongue detected different tastes. The map of the tongue, below, shows where different tastes were thought to be sensed.
But we now know this was far too simplistic and inaccurate. The entire tongue can taste equally in all areas.
The old explanation of where tastes were sensed didn’t explain how some foods could start out as sour and become sweet. Or how most of us overcome the bitter taste of coffee or the fiery burn of chili peppers. Researchers believe it is this intertwined taste in the papillae and pain nerves wrapped around them that actually creates flavor. In effect, the highly pleasurable part of flavor is actually due to the activation of pain receptors.
Why are taste and pain associated?
In the beginning we had to be able to differentiate nutritious from harmful foods. What we put in our mouth is the first line of defense. If we sense it may be harmful, pain receptors in the mouth and palate are activated that then transmit life savings signals to the brain in order to initiate a fight or flight response. It’s this perception of pain that keeps us from ingesting more, preventing further injury.
Making sure the acquisition of nutrients that fuel our body isn’t dangerous starts with taste. When the food creates a burning, irritation or pain sensation this unique combination of taste and pain activates a family of proteins called the transient receptor potential (TRP) channels. They reside within sensory tissue and play a pivotal role in signaling the brain data regarding taste, temperature, touch and nociception (pain). Nerve endings wrapped around the papilla of our taste buds specifically activate the TRPV1 receptors when they perceive a danger, signaling the brain to be aware.
Recent evidence suggests TRPs work by detecting oxidative stress- where free radicals build up as a result of the bodies inability to detoxify itself-and other markers of injury or inflammation that have caused tissue damage or injury. This then initiates a cascade of signals that lead to cellular repair, proliferation and survival. Studies show in some cases a sustained activation results, even after the inciting event has passed, causing the TRP channels to become dysfunctional. This then leads to persistent inflammation, neuropathic pain and in the case of our papillae, a decreased ability to detect taste- diminishing an important defensive mechanism.
Since the entire system is intertwined, anything that is perceived as causing heat, taste and/or pain can activate the same areas in the brain. Researchers have been especially interested in chili peppers as a possible route to new, more targeted pain treatments. Hot peppers trick the brain into thinking the mouth is on fire when there’s no actual heat. It’s because of the chemical in them- capsaicin. It binds to the painful nerve receptors, TRPV1, which then sends the same heat warning signals to the brain. The body responds by trying to cool itself- we sweat, our face turns red, eyes tear, nose runs… all mechanisms to remove the”threat.”
But capsaicin can also cause desensitization through the TRPV1 receptors by “irritating” the nerve endings and setting up a constant low level reaction that keeps the pain signals from transmitting. This involves calcium and sodium levels, as well as the depletion of certain substances over time. Another theory for this desensitization is that capsaicin causes so much calcium to be released it overwhelms the mitochondria within peripheral nerve endings which diminishes their hypersensitivity to pain.
This may be similar to how the body reacts when we eat chili peppers. Ever wonder how some people are more susceptible to spicy foods then others? Researchers noted that if you keep eating chilies their effect keeps building. But take even a two minute break and then eat one again you are somewhat desensitized. This may explain why some tolerate spices more than others, they establish a tolerance as they eat their meal. From chips and salsa to a few minutes later the main dish, that respite is enough to decrease the “heat” the body perceives. It may also explain why others who eat them all at once are overwhelmed and stop for good.
Another theory is that anything that causes the pain fibers to be activated also activates the release of our own endorphins and dopamine receptors, our own feel good hormones. The adage “hurts so good” couldn’t be truer. Not into jogging a mile to get a “runners high?” Try a few chili peppers instead.
Understanding that the neural circuitry that carries signals aversive taste also carries our response to pain opens up all sorts of new possibilities for pain management. As the role of the TRPs in chronic pain and how it’s modulated is better understood many of these channels show promise as therapeutic targets for managing pain. TRPV1 antagonists have been found to reduce inflammation and pain without the addictive side effects of opioids. Changing how these channels transmit taste messages might be the next great way to impact how pain signals are received as well.