7.4 Taste

Some insects have taste receptors on their feet, which allow them to taste what they are walking on. Fish have taste receptors not just in their mouths but all over their bodies (Hara, 1994). They can taste their prey before they see it, and they use taste to help them track it down. For us and other mammals, taste has a more limited but still valuable function. Our taste receptors exist only in our mouths, and their function is to help us decide whether a particular substance is good or bad to eat.

Anatomy and Physiology of Taste

The receptors for taste are found on specialized taste receptor cells, not directly on the sensory neurons (unlike the case for smell). These cells exist in spherical structures called taste buds. Each bud contains between 50 and 100 receptor cells, arranged something like segments in an orange (see Figure 7.6). Most people have between 2,000 and 10,000 taste buds, about two-thirds of which are on the tongue and the rest of which are on the roof of the mouth and in the opening of the throat (Herness & Gilbertson, 1999). People who have more taste buds are typically more sensitive to tastes—especially to bitter tastes—than are people who have fewer taste buds (Bartoshuk & Beauchamp, 1994).

Figure 7.6: A taste bud Taste buds are found in the surface tissue (epithelium) of the tongue and elsewhere in the mouth. Each one contains 50 or more taste receptor cells. From the tip of each cell, hair-like extensions make contact with the fluid lining the epithelial tissue. These extensions contain binding sites and channels where substances to be tasted exert their effects. The receptor cells produce action potentials in response to such input and, in turn, induce action potentials in taste sensory neurons through synaptic transmission

(Adapted from Herness & Gilbertson, 1999.)

To be tasted, a chemical substance must first dissolve in saliva and come into contact with the sensitive ends of appropriate taste receptor cells, where it triggers electrical changes that result in action potentials, first in the taste receptor cells and then, by synaptic transmission, in sensory neurons that run to the brain (see Figure 7.6). The specifics of the transduction mechanism vary from one type of taste receptor cell to another.

Five Primary Tastes, Five Types of Receptor Cells

For many years Western scientists believed that in humans (and other mammals) taste receptor cells were of just four types—sweet, salty, sour, and bitter. Every taste, it was believed, could be understood as a combination of those four primary tastes. Japanese scientists, in contrast, generally spoke of five primary tastes—the four just mentioned plus umami, which, loosely translated, means “savory” or “delicious” (Kurihara & Kashiwayanagi, 1998). Umami, they held, is a unique taste, unmatched by any combination of the other primary tastes, and is a major contributor to the taste of many natural foods, especially those that are high in protein, such as meats, fish, and cheese. Umami is also the taste produced by monosodium glutamate (MSG), an amino acid frequently used as a flavor enhancer in Asian cuisine. Taste researchers have recently identified distinct receptor cells and brain areas responsive to MSG, and now even Western taste specialists generally write of five rather than four primary tastes and types of taste receptor cells (Scott, 2012; Shadan, 2009).

Taste Areas in the Brain

Taste sensory neurons have strong connections (via several way stations) to the limbic system and cerebral cortex. The connections to the primary taste area of the cortex (located largely in the insula, which is buried in the central fissure that separates the temporal and parietal lobes) are arranged in such a way that different sets of neurons are selectively responsive to each of the five basic categories of taste stimuli (Kobayashi, 2006; Rolls, 2004). People with extensive damage to this area lose their conscious experience of taste (Pritchard, 1991), and artificial stimulation here produces experiences of taste in the absence of any stimuli on the tongue (Penfield & Faulk, 1955). The primary taste area in turn sends connections to several other areas of the cortex, including the orbitofrontal cortex, where, as mentioned in the section on smell, neural connections for taste and smell intermingle and enable us to experience the mixed taste–smell sensation called flavor.

Hmm, umami The savory umami taste of Asian food is often enhanced by monosodium glutamate. Umami is believed to be one of the five primary tastes.

Inga Nielsen/Shutterstock

An Evolutionary Account of Taste Quality

The purpose of taste is to motivate us to eat some substances and avoid eating others. Generally speaking, salty (at low to moderate intensity), sweet, and umami are pleasant tastes; in the course of evolution, they became attached to substances that are good for us, or at least were good for our evolutionary ancestors, given their nutritional needs and the environment in which they had to meet those needs. A certain amount of salt intake is needed to maintain a proper salt balance in bodily fluids. Sugars, in fruits and other natural foodstuffs, were a valuable source of energy to our evolutionary ancestors. Protein (the main natural source of umami flavor) is essential for building and restoring tissues. Our ability to taste and enjoy salt, sugars, and proteins is part of the mechanism that helps ensure that we consume adequate amounts of these nutrients.

Still speaking generally, sour and bitter are unpleasant experiences, which natural selection has attached to certain substances that are bad for us. Bacterial decay produces acidic compounds. Since decaying substances can cause disease when eaten, natural selection produced a taste system that experiences most acids as unpleasant (sour). Many bitter-tasting plants (hemlock is a famous example) and some animals (notably some species of caterpillars), as part of their own evolution, have concentrated toxic substances into their tissues—substances that can harm or kill animals that eat them. As a consequence, our ancestors evolved a taste system that experiences most of those toxic substances as unpleasant (bitter).

Evolution of the Ability to Taste Toxic Substances as Bitter

Yuck, bitter This response may protect children from eating poisonous substances. The mammalian taste system evolved to sense many poisons as bitter. Among humans, young children are especially sensitive to, and rejecting of, bitter taste.

© Kathleen Nelson/Alamy

To pursue this evolutionary line of thinking, let’s consider further the relationship between bitter taste and poisons. A wide variety of chemical substances all taste bitter to us, even though they may be very different chemically from one another, because each is able to bind to one or another of the approximately 25 different types of receptor sites located on bitter receptor cells (Behrens et al., 2007). The receptor sites are specialized protein molecules that bind certain molecules that come into contact with them. The binding of any substance to these sites triggers a chemical change in the cell. This chemical change results in action potentials in the sensory neurons and, ultimately, activity in areas of the brain that produce the bitter sensation.

From an evolutionary perspective it is no accident that there are so many different types of receptor sites on bitter receptor cells and that most of the chemicals they bind are either poisonous to us or chemically similar to poisons. Imagine an early species of animal that ate plants, some of which contain substance A, a poison that kills by interfering with the animal’s respiratory system. Any mutations affecting the taste system of an individual of this species in such a way as to make it dislike the taste of A would promote that individual’s survival and reproduction, so those new A-rejecting genes would multiply from generation to generation.

Individuals having the new genes would experience substance A as having a negative, bitter taste and would avoid it; but they would continue to eat plants that contain another poison, substance B, which kills animals by paralyzing the muscular system. Because B is an entirely different compound from A, it does not attach to the A receptors on the taste cells that trigger bitterness, so the animals have no sensory grounds for avoiding it. Now imagine a single mutation, which results in a new variety of receptor protein on the surface of bitter taste cells, a protein that can bind molecules of B. The animal with this mutation would experience the same bitter sensation upon eating leaves containing B as it experiences when eating leaves containing A, and it would avoid both of them. It would be more likely to survive and send progeny into the next generation than would other members of the species, and many of those progeny would inherit the new gene.

Extending this scenario, you can imagine how natural selection might have produced modern mammals that have bitter taste cells containing many different types of receptor proteins, able collectively to bind molecules of most toxic substances found in plants and other potential foods. We can’t go back and prove with certainty that this is how the present state of affairs relating to bitterness came about, but this account helps make sense of the facts of bitter taste.

Possible Explanation of Sex and Age Differences in Bitter Sensitivity

Although avoidance of bitter-tasting foods is generally adaptive, too much avoidance of them is not. Plants protect themselves from being eaten not just by producing truly poisonous substances, but also by producing nonpoisonous substances that are sufficiently similar to poisons that they bind to bitter taste receptors and produce bitter taste. Individuals that avoided all bitter tastes would lose the nutritional value of plants that taste bitter but are safe to eat. Through observation and experience, people and other plant-eating animals can learn to eat and enjoy bitter foods that have no toxins or low levels of toxins.

Among humans, women are generally more sensitive to bitter taste than are men. In fact, about 35 percent of women are said to be “supertasters,” with a special sensitivity to bitter taste. This is compared to about 15 percent of men, and about 25 percent of people cannot taste the specific bitter chemical at all (non-tasters). Supertasting (and the lack of it) seems to be controlled by a single dominant gene, with supertasters having an increased number of fungiform papillae on their tongues and (Bartoshuk et al., 1994, 1996) (see Figure 7.7).

Figure 7.7: Are you a supertaster? There’s an easy test you can do at home to find out. You’ll need (1) a thick piece paper, such as a 3 x 5 note card or a piece of construction paper; (2) a hole punch; (3) blue food coloring; (4) a mirror; and (5) a magnifying glass. Punch a hole on the paper with the hole punch (about 6 mm in diameter). Then, rub food coloring on your tongue. Although this will turn your tongue blue, the papillae will appear as pinkish bumps. Place the card over your tongue and press gently. Using the mirror and the magnifying glass, count the number of bumps (papillae) you see through the hole in the paper. If you count over 35 or 40 papillae, you’re a supertaster. If you count between 15 and 35, you’re a “medium taster.” And if you count fewer than 15, you’re a nontaster.

Courtesy of Linda Bartoshuk

Although women are generally more sensitive to bitter taste than men, many women become increasingly sensitive to it during the first 3 months of pregnancy (Duffy & Bartoshuk, 1996; Nordin et al., 2004). A possible reason is found in evidence that human fetuses are highly subject to damage by poisons, especially during the first 3 months of their development (Profet, 1992). With the stakes being survival of offspring, the value of avoiding even mild toxins increases.

Young children also appear to be highly sensitive to bitter tastes (Cowart, 1981), which may help explain why it is so difficult to get them to eat nutritious but bitter-tasting greens, such as spinach or Brussels sprouts. Children’s extra sensitivity to bitterness may help protect them from eating poisonous materials during their early development, before they have learned what is safe to eat and what is not.