Like our other senses, our audition, or hearing, helps us adapt and survive. For those of us who communicate invisibly—by shooting unseen air waves across space and receiving back the same—hearing provides information and enables relationships. Hearing loss is therefore an invisible disability. To not catch someone’s name, to not grasp what someone is asking, and to miss the hilarious joke is to be deprived of what others know, and sometimes to feel excluded. (As a person with hearing loss, I [DM] know the feeling.)

Most of us, however, can hear a wide range of sounds, and the ones we hear best are those in the range of the human voice. With normal hearing, we are remarkably sensitive to faint sounds, such as a child’s whimper. (If our ears were much more sensitive, we would hear a constant hiss from the movement of air molecules.) Our distant ancestors’ survival depended on this keen hearing when hunting or being hunted.

We are also remarkably attuned to sound variations. Among thousands of possible human voices, we easily recognize a friend on the phone, from the moment she says “Hi.” Moreover, hearing is fast. “It might take you a full second to notice something out of the corner of your eye, turn your head toward it, recognize it, and respond to it,” notes auditory neuroscientist Seth Horowitz (2012). “The same reaction to a new or sudden sound happens at least 10 times as fast.” A fraction of a second after such events stimulate the ear’s receptors, millions of neurons have simultaneously coordinated in extracting the essential features, comparing them with past experience, and identifying the stimulus (Freeman, 1991). For hearing as for our other senses, we wonder: How do we do it?

6-16 What are the characteristics of air pressure waves that we hear as sound?

Draw a bow across a violin, and you will unleash the energy of sound waves. Jostling molecules of air, each bumping into the next, create waves of compressed and expanded air, like the ripples on a pond circling out from a tossed stone. As we swim in our ocean of moving air molecules, our ears detect these brief air pressure changes.

Like light waves, sound waves vary in shape (FIGURE 6.36). The amplitude of sound waves determines their loudness. Their length, or frequency, determines the pitch we experience. Long waves have low frequency—and low pitch. Short waves have high frequency—and high pitch. Sound waves produced by a violin are much shorter and faster than those produced by a cello or a bass guitar.

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We measure sounds in decibels, with zero decibels representing the absolute threshold for hearing. Every 10 decibels correspond to a tenfold increase in sound intensity. Thus, normal conversation (60 decibels) is 10,000 times more intense than a 20-decibel whisper. And a temporarily tolerable 100-decibel passing subway train is 10 billion times more intense than the faintest detectable sound.

6-17 How does the ear transform sound energy into neural messages?

The intricate process that transforms vibrating air into nerve impulses, which our brain decodes as sounds, begins when sound waves enter the outer ear. An intricate mechanical chain reaction begins as the visible outer ear channels the waves through the auditory canal to the eardrum, a tight membrane, causing it to vibrate (FIGURE 6.37 below). In the middle ear, a piston made of three tiny bones (the hammer, anvil, and stirrup) picks up the vibrations and transmits them to the cochlea, a snail-shaped tube in the inner ear. The incoming vibrations cause the cochlea’s membrane (the oval window) to vibrate, jostling the fluid that fills the tube. This motion causes ripples in the basilar membrane, bending the hair cells lining its surface, not unlike the wind bending a wheat field. Hair cell movement triggers impulses in the adjacent nerve cells. Axons of those cells converge to form the auditory nerve, which sends neural messages (via the thalamus) to the auditory cortex in the brain’s temporal lobe. From vibrating air to moving piston to fluid waves to electrical impulses to the brain: Voila! We hear.

Perhaps the most intriguing part of the hearing process is the hair cells—“quivering bundles that let us hear” thanks to their “extreme sensitivity and extreme speed” (Goldberg, 2007). A cochlea has 16,000 of them, which sounds like a lot until we compare that with an eye’s 130 million or so photoreceptors. But consider their responsiveness. Deflect the tiny bundles of cilia on the tip of a hair cell by the width of an atom—the equivalent of displacing the top of the Eiffel Tower by half an inch—and the alert hair cell, thanks to a special protein at its tip, triggers a neural response (Corey et al., 2004).

Across the world, 360 million people are challenged by hearing loss (WHO, 2012). Damage to the cochlea’s hair cell receptors or their associated nerves can cause sensorineural hearing loss (or nerve deafness). Occasionally, disease damages these receptors, but more often the culprits are biological changes linked with heredity, aging, and prolonged exposure to ear-splitting noise or music. Sensorineural hearing loss is more common than conduction hearing loss, which is caused by damage to the mechanical system that conducts sound waves to the cochlea.

The cochlea’s hair cells have been likened to carpet fibers. Walk around on them and they will spring back with a quick vacuuming. But leave a heavy piece of furniture on them for a long time and they may never rebound. As a general rule, if we cannot talk over a noise, it is potentially harmful, especially if prolonged and repeated (Roesser, 1998). Such experiences are common when sound exceeds 100 decibels, as happens in venues from frenzied sports arenas to personal music systems playing near maximum volume (FIGURE 6.38 below). Ringing in the ears after exposure to loud sounds indicates that we have been bad to our unhappy hair cells. One study of teen rock concert attendees found that after three hours of sound averaging 99 decibels, 54 percent reported not hearing as well, and 1 in 4 had ringing in their ears. As pain alerts us to possible bodily harm, ringing of the ears alerts us to possible hearing damage. It is hearing’s equivalent of bleeding.

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The rate of teen hearing loss, now 1 in 5, has risen by a third since the early 1990s (Shargorodsky et al., 2010). Teen boys more than teen girls or adults blast themselves with loud volumes for long periods (Zogby, 2006). Males’ greater noise exposure may help explain why men’s hearing tends to be less acute than women’s. But male or female, those who spend many hours in a loud nightclub, behind a power mower, or above a jackhammer should wear earplugs. “Condoms or, safer yet, abstinence,” say sex educators. “Earplugs or walk away,” say hearing educators.

For now, the only way to restore hearing for people with nerve deafness is a sort of bionic ear—a cochlear implant, which, by 2011, had been given to 219,000 people worldwide (NIDCD, 2013). This electronic device translates sounds into electrical signals that, wired into the cochlea’s nerves, convey information about sound to the brain. Cochlear implants given to deaf kittens and human infants have seemed to trigger an “awakening” of the pertinent brain area (Klinke et al., 1999; Sireteanu, 1999). These devices can help children become proficient in oral communication (especially if they receive them as preschoolers or even before age 1) (Dettman et al., 2007; Schorr et al., 2005). Cochlear implants can help restore hearing for most adults, but only if their brain learned to process sound during childhood.

6-18 How do we detect loudness, discriminate pitch, and locate sounds?

Responding to Loud and Soft Sounds How do we detect loudness? If you guessed that it’s related to the intensity of a hair cell’s response, you’d be wrong. Rather, a soft, pure tone activates only the few hair cells attuned to its frequency. Given louder sounds, neighboring hair cells also respond. Thus, your brain interprets loudness from the number of activated hair cells.

If a hair cell loses sensitivity to soft sounds, it may still respond to loud sounds. This helps explain another surprise: Really loud sounds may seem loud to people with or without normal hearing. As a person with hearing loss, I [DM] used to wonder what really loud music must sound like to people with normal hearing. Now I realize it sounds much the same; where we differ is in our perception of soft sounds. This is why we hard-of-hearing people do not want all sounds (loud and soft) amplified. We like sound compressed, which means harder-to-hear sounds are amplified more than loud sounds (a feature of today’s digital hearing aids).

Hearing Different Pitches How do we know whether a sound is the high-frequency, high-pitched chirp of a bird or the low-frequency, low-pitched roar of a truck? Current thinking on how we discriminate pitch combines two theories.

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Locating Sounds Why don’t we have one big ear—perhaps above our one nose? “The better to hear you,” as the wolf said to Red Riding Hood. Thanks to the placement of our two ears, we enjoy stereophonic (“three-dimensional”) hearing. Two ears are better than one for at least two reasons (FIGURE 6.39). If a car to your right honks, your right ear will receive a more intense sound, and it will receive the sound slightly sooner than your left ear.

Because sound travels 750 miles per hour and human ears are but 6 inches apart, the intensity difference and the time lag are extremely small. A just noticeable difference in the direction of two sound sources corresponds to a time difference of just 0.000027 second! Lucky for us, our supersensitive auditory system can detect such minute differences (Brown & Deffenbacher, 1979; Middlebrooks & Green, 1991).

Our brain gives seeing and hearing priority in the allocation of cortical tissue. But extraordinary happenings also occur within our other senses. Sharks and dogs rely on their outstanding sense of smell, aided by large brain areas devoted to this system. Without our senses of touch, taste, smell, and body position and movement, we humans would be seriously handicapped, and our capacities for enjoying the world would be greatly diminished.

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6-19 How do we sense touch?

Touch is vital. Right from the start, touch aids our development. Infant rats deprived of their mother’s grooming produce less growth hormone and have a lower metabolic rate—a good way to keep alive until the mother returns, but a reaction that stunts growth if prolonged. Infant monkeys allowed to see, hear, and smell—but not touch—their mother become desperately unhappy; those separated by a screen with holes that allow touching are much less miserable. Premature human babies gain weight faster and go home sooner if they are stimulated by hand massage (Field et al., 2006). As adults, we still yearn to touch—to kiss, to stroke, to snuggle. In experiments, strangers separated by a curtain, using their hands to touch only each other’s forearms, have been able to communicate anger, fear, disgust, love, gratitude, and sympathy at levels well above chance (Hertenstein et al., 2006).

Humorist Dave Barry was perhaps right to jest that your skin “keeps people from seeing the inside of your body, which is repulsive, and it prevents your organs from falling onto the ground.” But skin does much more. Touching various spots on the skin with a soft hair, a warm or cool wire, and the point of a pin reveals that some spots are especially sensitive to pressure, others to warmth, others to cold, still others to pain. Our “sense of touch” is actually a mix of these four basic and distinct skin senses, and our other skin sensations are variations of pressure, warmth, cold, and pain: Some examples:

Touch sensations involve more than tactile stimulation, however. A self-administered tickle produces less somatosensory cortex activation than does the same tickle from something or someone else (Blakemore et al., 1998). Likewise, a sensual leg caress evokes a different somatosensory cortex response when a heterosexual man believes it comes from an attractive woman rather than a man (Gazzola et al., 2012). Our responses to tickles and caresses reveal how quickly cognition influences our brain’s sensory response.

6-20 What biological, psychological, and social-cultural influences affect our experience of pain? How do placebos, distraction, and hypnosis help control pain?

Be thankful for occasional pain. Pain is your body’s way of telling you something has gone wrong. By drawing your attention to a burn, a break, or a sprain, pain orders you to change your behavior—“Stay off that turned ankle!” The rare people born without the ability to feel pain may experience severe injury or even death before early adulthood. Without the discomfort that makes us occasionally shift position, their joints fail from excess strain. Without the warnings of pain, the effects of unchecked infections and injuries accumulate (Neese, 1991).

More numerous are those who live with chronic pain, which is rather like an alarm that won’t shut off. The suffering of such people, and of those with persistent or recurring backaches, arthritis, headaches, and cancer-related pain, prompts two questions: What is pain? How might we control it?

Understanding Pain Our pain experiences vary widely. Women are more sensitive to pain than men are (their senses of hearing and smell also tend to be more sensitive) (Ruau et al., 2011; Wickelgren, 2009). Our individual pain sensitivity varies, too, depending on genes, physiology, experience, attention, and surrounding culture (Gatchel et al., 2007; Reimann et al., 2010). Thus, our experience of pain reflects both bottom-up sensations and top-down cognition.

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BIOLOGICAL INFLUENCES There is no one type of stimulus that triggers pain (as light triggers vision). Instead, there are different nociceptors—sensory receptors in our skin, muscles, and organs that detect hurtful temperatures, pressure, or chemicals (FIGURE 6.41).

Although no theory of pain explains all available findings, psychologist Ronald Melzack and biologist Patrick Wall’s (1965, 1983; Melzack & Katz, 2013) classic gate-control theory provides a useful model. The spinal cord contains small nerve fibers that conduct most pain signals, and larger fibers that conduct most other sensory signals. Melzack and Wall theorized that the spinal cord contains a neurological “gate.” When tissue is injured, the small fibers activate and open the gate, and you feel pain. Large-fiber activity closes the gate, blocking pain signals and preventing them from reaching the brain. Thus, one way to treat chronic pain is to stimulate (by massage, electric stimulation, or acupuncture) “gate-closing” activity in the large neural fibers (Wall, 2000).

But pain is not merely a physical phenomenon of injured nerves sending impulses to a definable brain area—like pulling on a rope to ring a bell. Melzack and Wall noted that brain-to-spinal-cord messages can also close the gate.

The brain can also create pain, as it does in people’s experiences of phantom limb sensations, after a limb has been amputated. Their brain may misinterpret the spontaneous central nervous system (CNS) activity that occurs in the absence of normal sensory input. As the dreamer may see with eyes closed, so 7 in 10 such people may feel pain or movement in nonexistent limbs (Melzack, 1992, 2005). (Some may also try to step off a bed onto a phantom limb or to lift a cup with a phantom hand.) Even those born without a limb sometimes perceive sensations from the absent arm or leg. The brain, Melzack (1998) has surmised, comes prepared to anticipate “that it will be getting information from a body that has limbs.”

Phantoms may haunt other senses too, as the brain, responding to the absence of sensory signals, amplifies irrelevant neural activity. People with hearing loss often experience the sound of silence: tinnitus, the phantom sound of ringing in the ears. Those who lose vision to glaucoma, cataracts, diabetes, or macular degeneration may experience phantom sights—nonthreatening hallucinations (Ramachandran & Blakeslee, 1998). Others who have nerve damage in the systems for tasting and smelling have experienced phantom tastes or smells, such as ice water that seems sickeningly sweet or fresh air that reeks of rotten food (Goode, 1999). The point to remember: We feel, see, hear, taste, and smell with our brain, which can sense even without functioning senses.

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PSYCHOLOGICAL INFLUENCES One powerful influence on our perception of pain is the attention we focus on it. Athletes, focused on winning, may play through the pain. Halfway through his lap of the 2012 Olympics 1600 meter relay, Manteo Mitchell broke one of his leg bones—and kept running.

We also seem to edit our memories of pain, which often differ from the pain we actually experienced. In experiments, and after medical procedures, people overlook a pain’s duration. Their memory snapshots instead record two factors: their pain’s peak moment (which can lead them to recall variable pain, with peaks, as worse [Stone et al., 2005]), and how much pain they felt at the end. In one experiment, researchers asked people to immerse one hand in painfully cold water for 60 seconds, and then the other hand in the same painfully cold water for 60 seconds followed by a slightly less painful 30 seconds more (Kahneman et al., 1993). Which experience would you expect to recall as most painful?

Curiously, when asked which trial they would prefer to repeat, most preferred the 90- second trial, with more net pain—but less pain at the end. Physicians have used this principle with patients undergoing colon exams—lengthening the discomfort by a minute, but lessening its intensity (Kahneman, 1999). Although the extended milder discomfort added to their net pain experience, patients experiencing this taper-down treatment later recalled the exam as less painful than did those whose pain ended abruptly. (If, at the end of a painful root canal, the oral surgeon asks if you’d like to go home or to have a few more minutes of milder discomfort, there’s a case to be made for prolonging your hurt.)

The end of an experience can color our memory of pleasures, too. In one simple experiment, some people, on receiving a fifth and last piece of chocolate, were told it was their “next” one. Others, told it was their “last” piece, liked it better and also rated the whole experiment as being more enjoyable (O’Brien & Ellsworth, 2012). Endings matter.

SOCIAL-CULTURAL INFLUENCES Our perception of pain varies with our social situation and our cultural traditions. We tend to perceive more pain when others seem to be experiencing pain (Symbaluk et al., 1997). This may help explain other apparent social aspects of pain, as when pockets of Australian keyboard operators during the mid-1980s suffered outbreaks of severe pain while typing or performing other repetitive work—without any discernible physical abnormalities (Gawande, 1998). Sometimes the pain in sprain is mainly in the brain—literally. When people felt empathy for another’s pain, their own brain activity partly mirrored the activity in the actual brain in pain (Singer et al, 2004).

Thus, our perception of pain is a biopsychosocial phenomenon (Hadjistavropoulos et al., 2011). Viewing pain from many perspectives can help us better understand how to cope with it and treat it (FIGURE 6.42).

Controlling Pain If pain is where body meets mind—if it is both a physical and a psychological phenomenon—then it should be treatable both physically and psychologically. Depending on the patient’s symptoms, pain control clinics select one or more therapies from a list that includes drugs, surgery, acupuncture, electrical stimulation, massage, exercise, hypnosis, relaxation training, and thought distraction.

That explains some striking influences on pain. When we are distracted from pain (a psychological influence) and soothed by the release of our naturally painkilling endorphins (a biological influence), our experience of pain diminishes. Sports injuries may go unnoticed until the after-game shower. People who carry a gene that boosts the availability of endorphins are less bothered by pain, and their brain is less responsive to pain (Zubieta et al., 2003). Others, who carry a mutated gene that disrupts pain circuit neurotransmission, may be unable to experience pain (Cox et al., 2006). Such discoveries could point the way toward new pain medications that mimic these genetic effects.

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PLACEBOS Even an inert placebo can help, by dampening the central nervous system’s attention and responses to painful experiences—mimicking analgesic drugs (Eippert et al., 2009; Wager & Atlas, 2013). After being injected in the jaw with a stinging saltwater solution, men in one experiment received a placebo said to relieve pain, and they immediately felt better. Being given fake painkilling chemicals caused the brain to dispense real ones, as indicated by activity in an area that releases natural painkilling opiates (Scott et al., 2007; Zubieta et al., 2005). “Believing becomes reality,” noted one commentator (Thernstrom, 2006), as “the mind unites with the body.”

Another experiment pitted two placebos—fake pills and pretend acupuncture—against each other (Kaptchuk et al., 2006). People with persistent arm pain received either sham acupuncture (with trick needles that retracted without puncturing the skin) or blue cornstarch pills that looked like a medication often prescribed for strain injury. A fourth of those receiving the nonexistent needle pricks and 31 percent of those receiving the fake pills complained of side effects, such as painful skin or dry mouth and fatigue. After two months, both groups were reporting less pain, with the fake acupuncture group reporting the greater pain drop.

DISTRACTION Distracting people with pleasant images (“Think of a warm, comfortable environment”) or drawing their attention away from the painful stimulation (“Count backward by 3’s”) is an effective way to activate pain-inhibiting circuits and to increase pain tolerance (Edwards et al., 2009). A well-trained nurse may distract needle-shy patients by chatting with them and asking them to look away when inserting the needle. Burn victims receiving excruciating wound care can benefit from an even more effective distraction: immersion in a computer-generated 3-D world, like the snow scene in FIGURE 6.43. Functional MRI (fMRI) scans have revealed that playing in the virtual reality reduces the brain’s pain-related activity (Hoffman, 2004). Because pain is in the brain, diverting the brain’s attention may bring relief. Better yet, research suggests, maximize pain relief by combining a placebo with distraction (Buhle et al., 2012), and amplify their effects with hypnosis. Hypnosis can also divert attention (see Thinking Critically About: Hypnosis and Pain Relief).

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6-21 In what ways are our senses of taste and smell similar, and how do they differ?

Like touch, our sense of taste involves several basic sensations. Taste’s sensations were once thought to be sweet, sour, salty, and bitter, with all others stemming from mixtures of these four (McBurney & Gent, 1979). Then, as investigators searched for specialized nerve fibers for the four taste sensations, they encountered a receptor for what we now know is a fifth—the savory meaty taste of umami, best experienced as the flavor enhancer monosodium glutamate (MSG).

Tastes exist for more than our pleasure (see TABLE 6.2). Pleasureful tastes attracted our ancestors to energy-or protein-rich foods that enabled their survival. Aversive tastes deterred them from new foods that might be toxic. We see the inheritance of this biological wisdom in today’s 2- to 6-year-olds, who are typically fussy eaters, especially when offered new meats or bitter-tasting vegetables, such as spinach and brussels sprouts (Cooke et al., 2003). Meat and plant toxins were both potentially dangerous sources of food poisoning for our ancestors, especially for children. Given repeated small tastes of disliked new foods, however, most children begin to accept them (Wardle et al., 2003). We come to like what we eat. Compared with breast-fed babies, German babies bottle fed vanilla-flavored milk grew up to be adults with a striking preference for vanilla flavoring (Haller et al., 1999).

Taste is a chemical sense. Inside each little bump on the top and sides of your tongue are 200 or more taste buds, each containing a pore that catches food chemicals. In each taste bud pore, 50 to 100 taste receptor cells project antenna-like hairs that sense food molecules. Some receptors respond mostly to sweet-tasting molecules, others to salty-, sour-, umami-, or bitter-tasting ones. It doesn’t take much to trigger a response that alerts your brain’s temporal lobe. If a stream of water is pumped across your tongue, the addition of a concentrated salty or sweet taste for but one-tenth of a second will get your attention (Kelling & Halpern, 1983). When a friend asks for “just a taste” of your soft drink, you can squeeze off the straw after a mere instant.

Taste receptors reproduce themselves every week or two, so if you burn your tongue with hot food it hardly matters. However, as you grow older, the number of taste buds decreases, as does taste sensitivity (Cowart, 1981). (No wonder adults enjoy strong-tasting foods that children resist.) Smoking and alcohol use accelerate these declines. Those who have lost their sense of taste have reported that food tastes like “straw” and is hard to swallow (Cowart, 2005).

Essential as taste buds are, there’s more to taste than meets the tongue. Expectations can influence taste. When told a sausage roll was “vegetarian,” people in one experiment found it decidedly inferior to its identical partner labeled “meat” (Allen et al., 2008). In another experiment, being told that a wine cost $90 rather than its real $10 price made it taste better and triggered more activity in a brain area that responds to pleasant experiences (Plassmann et al., 2008).

Life begins with an inhale and ends with an exhale. Between birth and death, you will daily inhale and exhale nearly 20,000 breaths of life-sustaining air, bathing your nostrils in a stream of scent-laden molecules. The resulting experiences of smell (olfaction) are strikingly intimate: You inhale something of whatever or whoever it is you smell.

Like taste, smell is a chemical sense. We smell something when molecules of a substance carried in the air reach a tiny cluster of 20 million receptor cells at the top of each nasal cavity (FIGURE 6.44). These olfactory receptor cells, waving like sea anemones on a reef, respond selectively—to the aroma of a cake baking, to a wisp of smoke, to a friend’s fragrance. Instantly, they alert the brain through their axon fibers. Being part of an old, primitive sense, olfactory neurons bypass the brain’s sensory control center, the thalamus.

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Even nursing infants and their mothers have a literal chemistry to their relationship. They quickly learn to recognize each other’s scents (McCarthy, 1986). Aided by smell, a mother fur seal returning to a beach crowded with pups will find her own. Our human sense of smell is less acute than our senses of seeing and hearing. Looking out across a garden, we see its forms and colors in exquisite detail and hear a variety of birds singing, yet we smell little of it without sticking our nose into the blossoms.

Odor molecules come in many shapes and sizes—so many, in fact, that it takes many different receptors to detect them. A large family of genes designs the 350 or so receptor proteins that recognize particular odor molecules (Miller, 2004). Linda Buck and Richard Axel (1991) discovered (in work for which they received a 2004 Nobel Prize) that these receptor proteins are embedded on the surface of nasal cavity neurons. As a key slips into a lock, so odor molecules slip into these receptors. Yet we don’t seem to have a distinct receptor for each detectable odor. Odors trigger combinations of receptors, in patterns that are interpreted by the olfactory cortex. As the English alphabet’s 26 letters can combine to form many words, so odor molecules bind to different receptor arrays, producing at least 1 trillion odors that we could potentially discriminate (Bushdid et al., 2014). It is the combinations of olfactory receptors, which activate different neuron patterns, that allow us to distinguish between the aromas of fresh-brewed and hours-old coffee (Zou et al., 2005).

Gender and age influence our ability to identify scents. Women and young adults have the best sense of smell (Wickelgren, 2009; Wysocki & Gilbert, 1989). Physical condition also matters. Smokers and people with Alzheimer’s disease, Parkinson’s disease, or alcohol use disorder typically have a diminished sense of smell (Doty, 2001). For all of us, however, the sense of smell tends to peak in early adulthood and gradually declines thereafter (FIGURE 6.45 below).

Despite our skill at discriminating scents, we aren’t very good at describing them. Try it: Which is easier, describing the sound of coffee brewing, or the aroma of coffee? For most people, it’s the sound. Compared with how we experience and remember sights and sounds, smells are primitive and harder to describe and recall (Richardson & Zucco, 1989; Zucco, 2003).

As any dog or cat with a good nose could tell us, we each have our own identifiable chemical signature. (One noteworthy exception: A dog will follow the tracks of one identical twin as though they had been made by the other [Thomas, 1974].) Animals that have many times more olfactory receptors than we do also use their sense of smell to communicate and to navigate. Long before a shark can see its prey, or a moth its mate, olfactory cues direct their way, as they also do for migrating salmon returning to their home stream. After being exposed in a hatchery to one of two odorant chemicals, salmon have, when returning two years later, sought whichever stream near their release site was spiked with the familiar smell (Barinaga, 1999).

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For humans, too, the attractiveness of smells depends on learned associations (Herz, 2001). As babies nurse, their preference for the smell of their mother’s breast builds. So, too, with other associations. As good experiences are linked with a particular scent, people come to like that scent. This helps explain why people in the United States tend to like the smell of wintergreen (which they associate with candy and gum) more than do those in Great Britain (where it often is associated with medicine). In another example of odors evoking unpleasant emotions, researchers frustrated Brown University students with a rigged computer game in a scented room (Herz et al., 2004). Later, if exposed to the same odor while working on a verbal task, the students’ frustration was rekindled and they gave up sooner than others exposed to a different odor or no odor.

Though it’s difficult to recall odors by name, we may recognize long-forgotten odors and their associated memories (Engen, 1987; Schab, 1991). The smell of the sea, the scent of a perfume, or an aroma of a favorite relative’s kitchen can bring to mind a happy time. It’s a phenomenon the British travel agent chain Lunn Poly understood well. To evoke memories of relaxing on sunny, warm beaches, the company once piped the aroma of coconut suntan oil into its shops (Fracassini, 2000).

Our brain’s circuitry helps explain an odor’s power to evoke feelings and memories (FIGURE 6.46). A hotline runs between the brain area receiving information from the nose and the brain’s ancient limbic centers associated with memory and emotion. Thus, when put in a foul-smelling room, people expressed harsher judgments of immoral acts (such as lying or keeping a found wallet) and more negative attitudes toward gay men (Inbar et al., 2011; Schnall et al., 2008). Exposed to a fishy smell during a trust game, people become more suspicious (Lee & Schwarz, 2012). And when riding on a train car with the citrus scent of a cleaning product, people have left behind less trash (de Lange et al., 2012).

Smell is indeed primitive. Eons before the elaborate analytical areas of our cerebral cortex had fully evolved, our mammalian ancestors sniffed for food—and for predators. When running in the Republican primary to select a candidate in the next election of a governor of New York, Carl Paladino understood that primitive, disgusting smells can affect judgments. He mailed a flyer that smelled of rotting garbage with a message attacking his opponent—whom he then defeated 62 to 38 percent (Liberman & Pizarro, 2010).

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6-22 How do we sense our body’s position and movement?

Important sensors in your joints, tendons, and muscles enable your kinesthesia—your sense of the position and movement of your body parts. By closing your eyes or plugging your ears you can momentarily imagine being without sight or sound. But what would it be like to live without touch or kinesthesia—without, therefore, being able to sense the positions of your limbs when you wake during the night? Ian Waterman of Hampshire, England, knows. In 1972, at age 19, Waterman contracted a rare viral infection that destroyed the nerves enabling his sense of light touch and of body position and movement. People with this condition report feeling disembodied, as though their body is dead, not real, not theirs (Sacks, 1985). With prolonged practice, Waterman learned to walk and eat—by visually focusing on his limbs and directing them accordingly. But if the lights go out, he crumples to the floor (Azar, 1998). Even for the rest of us, vision interacts with kinesthesia. Stand with your right heel in front of your left toes. Easy. Now close your eyes and you will probably wobble.

A companion vestibular sense monitors your head’s (and thus your body’s) position and movement. The biological gyroscopes for this sense of equilibrium are two structures in your inner ear. The first, your semicircular canals, look like a three-dimensional pretzel (see FIGURE 6.37a). The second, connecting those canals with the cochlea, is the pair of vestibular sacs, which contain fluid that moves when your head rotates or tilts. When this movement stimulates hair-like receptors, sending messages to the cerebellum at the back of your brain, you sense your body position and maintain your balance.

If you twirl around and then come to an abrupt halt, neither the fluid in your semicircular canals nor your kinesthetic receptors will immediately return to their neutral state. The dizzy aftereffect fools your brain with the sensation that you’re still spinning. This illustrates a principle that underlies perceptual illusions: Mechanisms that normally give us an accurate experience of the world can, under special conditions, fool us. Understanding how we get fooled provides clues to how our perceptual system works.

6-23 How does sensory interaction influence our perceptions, and what is embodied cognition?

Our senses—seeing, hearing, tasting, smelling, touching—eavesdrop on one another (Rosenblum, 2013). In interpreting the world, our brain blends their inputs. Consider what happens to your sense of taste if you hold your nose, close your eyes, and have someone feed you various foods. A slice of apple may be indistinguishable from a chunk of raw potato. A piece of steak may taste like cardboard. Without their smells, a cup of cold coffee may be hard to distinguish from a glass of red wine. Our sense of smell sticks its nose into the business of taste.

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Thus, to savor a taste, we normally breathe the aroma through our nose—which is why eating is not much fun when you have a bad cold. Smell can also change our perception of taste: A drink’s strawberry odor enhances our perception of its sweetness. Depending on its texture, a potato chip “tastes” fresh or stale (Smith, 2011). This is sensory interaction at work—the principle that one sense may influence another. Smell + texture + taste = flavor. Yet, despite the nose’s contribution of smell, flavor feels located in the mouth (Stevenson, 2014).

Vision and hearing may similarly interact. A weak flicker of light that we have trouble perceiving becomes more visible when accompanied by a short burst of sound (Kayser, 2007). And a sound may be easier to hear with a visual cue. If I [DM], as a person with hearing loss, watch a video with simultaneous captioning, I have no trouble hearing the words I am seeing. I may therefore think I don’t need the captioning, but if I then turn off the captioning, I suddenly realize I do need it. The eyes guide the ears (FIGURE 6.47).

But what do you suppose happens if the eyes and the ears disagree? What if we see a speaker saying one syllable while we hear another? Surprise: We may perceive a third syllable that blends both inputs. Seeing the mouth movements for ga while hearing ba we may perceive da. This phenomenon is known as the McGurk effect, after its discoverers, Scottish psychologist Harry McGurk and his assistant John MacDonald (1976). For all of us, lip reading is part of hearing.

Touch also interacts with our other senses. In detecting events, the brain can combine simultaneous touch and visual signals, thanks to neurons projecting from the somatosensory cortex back to the visual cortex (Macaluso et al., 2000). Touch even interacts with hearing. One experiment blew a puff of air (such as our mouths produce when saying pa and ta) on the neck or hands as people heard either these sounds or the more airless sounds ba or da. The result? People more often misheard ba or da as pa or ta when played with the faint puff (Gick & Derrick, 2009). Thanks to sensory interaction, they heard with their skin.

Our brain even blends our tactile and social judgments, as demonstrated in these playful experiments:

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These examples of embodied cognition illustrate how brain circuits processing bodily sensations connect with brain circuits responsible for cognition. We think from within a body.

So, the senses interact: As we attempt to decipher our world, our brain blends inputs from multiple channels. For many people, an odor, perhaps of mint or chocolate, can evoke a sensation of taste (Stevenson & Tomiczek, 2007). But in a few select individuals, the senses become joined in a phenomenon called synesthesia, where one sort of sensation (such as hearing sound) involuntarily produces another (such as seeing color). Early in life, “exuberant neural connectivity” produces some arbitrary associations among the senses, which later are normally—but not always—pruned (Wagner & Dobkins, 2011). Thus, hearing music may activate color-sensitive cortex regions and trigger a sensation of color (Brang et al., 2008; Hubbard et al., 2005). Seeing the number 3 may evoke a taste sensation (Ward, 2003). Those who experience such sensory shifts are known as synesthetes.

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For a summary of our sensory systems, see TABLE 6.3. The river of perception is fed by sensation, cognition, and emotion. And that is why we need biological, psychological, and social-cultural levels of analysis (FIGURE 6.48).

If perception is the product of these three sources, what can we say about extrasensory perception, which claims that perception can occur apart from sensory input? For more on that question, see Thinking Critically About: ESP—Perception Without Sensation?

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To feel awe, mystery, and a deep reverence for life, we need look no further than our own perceptual system and its capacity for organizing formless nerve impulses into colorful sights, vivid sounds, and evocative smells. As Shakespeare’s Hamlet recognized, “There are more things in Heaven and Earth, Horatio, than are dreamt of in your philosophy.” Within our ordinary sensory and perceptual experiences lies much that is truly extraordinary—surely much more than has so far been dreamt of in our psychology.

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