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The Teenage Brain: A neuroscientist’s survival guide to raising adolescents and young adults
The Teenage Brain: A neuroscientist’s survival guide to raising adolescents and young adults
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The Teenage Brain: A neuroscientist’s survival guide to raising adolescents and young adults

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These are a few of things I say to parents right off the bat: The sense of whiplash you are feeling is not unusual. Your children are changing, and also trying to figure themselves out; their brains and bodies are undergoing extensive reorganization; and their apparent recklessness, rudeness, and cluelessness are not totally their fault! Almost all of this is neurologically, psychologically, and physiologically explainable. As a parent or educator, you need to remind yourself of this daily, often hourly!

Adolescence is a minefield, for sure. It is also a relatively recent “discovery.” The idea of adolescence as a general period of human development has been around for aeons, but as a discrete period between childhood and adulthood it can be traced back only as far as the middle of the twentieth century. In fact the word “teenager,” (#litres_trial_promo) as a way of describing this distinct stage between the ages of thirteen and nineteen, first appeared in print, and only in passing, in a magazine article in April 1941.

Mostly for economic reasons, children were considered miniadults well into the nineteenth century. They were needed to sow the fields, milk the cows, and split the firewood. By the time of the American Revolution half the population of the new colonies was under the age of sixteen. If a girl was still single at eighteen, she was considered virtually unmarriageable. Well into the early twentieth century, children over the age of ten, and often children much younger, were capable of most kinds of work, either on the farm or later in city factories—even if they needed boxes to stand on. By 1900, with the Industrial Revolution in full swing, more than two million children were employed in the United States.

Two things in the decades spanning the middle of the twentieth century—the Great Depression and the rise of high schools—not only changed attitudes about the meaning of childhood but also helped to usher in the era of the teenager. With the onset of the Depression (#litres_trial_promo) after the stock market crash of 1929, child laborers were the first to lose their jobs. The only other place for them was school, which is why by the end of the 1930s, and for the first time in the history of American education, most fourteen- to seventeen-year-olds were enrolled in high school. Even today, according to a 2003 survey by the National Opinion Research Center, Americans regard finishing high school as the number one hallmark of adulthood (#litres_trial_promo). (In much of the United Kingdom a teenager is treated as an adult even if he or she does not finish high school, and in England, Scotland, and Wales it is legal not only to leave school at age sixteen but to leave home and live independently as well.) In the 1940s and ’50s, American youth, most of whom were not responsible for the economic survival of their families, certainly did not seem like adults—at least not until they graduated from high school. They generally lived at home and were dependent on their parents, and as more and more children found themselves going to school beyond the eighth grade, they became a kind of class unto themselves. They looked different from adults, dressed differently, had different interests, even a different vocabulary. In short, they were a new culture. As one anonymous writer said at the time, “Young people became teenagers (#litres_trial_promo) because we had nothing better for them to do.”

One man foresaw it all more than one hundred years ago. The American psychologist Granville Stanley Hall never used the word “teenager” in his groundbreaking 1904 book about youth culture, but it was clear from the title of his fourteen-hundred-page tome—Adolescence: Its Psychology and Its Relations to Physiology, Anthropology, Sociology, Sex, Crime, Religion and Education—that he regarded the time between childhood and adulthood as a discrete developmental stage. To Hall, who was the first American to earn a PhD in psychology, from Harvard University, and the first president of the American Psychological Association, adolescence was a peculiar time of life, a distinct and separate stage qualitatively different from either childhood or adulthood. Adulthood, he said, was akin to the fully evolved man of reason; childhood a time of savagery; and adolescence a period of wild exuberance, which he described as primitive, or “neo-atavistic,” and therefore only slightly more controlled than the absolute anarchy of childhood.

Hall’s suggestion to parents and educators: Adolescents shouldn’t be coddled but rather should be corralled, then indoctrinated with the ideals of public service, discipline, altruism, patriotism, and respect for authority. If Hall was somewhat provincial about how to treat adolescent storm and stress, he was nonetheless a pioneer in suggesting a biological connection between adolescence and puberty and even used language that presaged neuroscientists’ later understanding of the malleability of the brain, or “plasticity.” “Character and personality are taking form (#litres_trial_promo), but everything is plastic,” he wrote, referring to pliability, not the man-made product. “Self-feeling and ambition are increased, and every trait and faculty is liable to exaggeration and excess.”

Self-feeling, ambition, exaggeration, and excess—they all helped define “teenager” for the American public in the middle of the twentieth century. The teenager as a kind of cultural phenomenon took off in the post-World War II era—from teenyboppers and bobbysoxers to James Dean in Rebel Without a Cause and Holden Caulfield in The Catcher in the Rye. But while the age of adolescence became more defined and accepted, the demarcation between childhood and adulthood remained—and remains—slippery. As a society, we still carry the vestiges of our centuries-old confusion about when a person should be considered an adult. In most of the United States a person must be between fifteen and seventeen to drive; eighteen to vote, buy cigarettes, and join the military; twenty-one to drink alcohol; and twenty-five to rent a car. The minimum age to be a member of the House of Representatives is twenty-five; to be president of the United States, thirty-five; and the minimum age to be a governor ranges among states from no age restriction at all (six states) to a minimum age of thirty-one (Oklahoma). There is generally no minimum age requirement to testify in most courts, enter into a contract or sue, request emancipation from one’s parents, or seek alcohol or drug treatment. But you must be eighteen to determine your own medical care or write a legally binding will, and in at least thirty-five states those eighteen or younger must have some type of parental involvement before undergoing an abortion. What a lot of mixed messages we give these teenagers, who are not at a stage to weed through the logic (if there is any) behind how society holds them accountable. Very confusing.

So what does being a teenager mean? Man-child, woman-child, quasi-adult? The question is about much more than semantics, philosophy, or even psychology because the repercussions are both serious and practical for parents, educators, and doctors, as well as the criminal justice system, not to mention teens themselves.

Hall, for one, believed adolescence began with the initiation of puberty, and this is why he is considered the founder of the scientific study of adolescence. Although he had no empirical evidence for the connection, Hall knew that understanding the mental, emotional, and physical changes that happen in a child’s transition into adulthood could come only from an understanding of the biological mechanics of puberty.

One of the chief areas of focus in the study of puberty has long been “hormones,” but hormones have gotten a bad rap with parents and educators, who tend to blame them for everything that goes wrong with teenagers. I always thought the expression “raging hormones” made it seem as though these kids had taken a wicked potion or cocktail that made them act with wild disregard for anyone and anything. But we are truly blaming the messenger when we cite hormones as the culprit. Think about it: When your three-year-old has a temper tantrum, do you blame it on raging hormones? Of course not. We know, simply, that three-year-olds haven’t yet figured out how to control themselves.

In some ways, that’s true of teenagers as well. And when it comes to hormones, the most important thing to remember is that the teenage brain is “seeing” these hormones for the first time. Because of that, the brain hasn’t yet figured out how to modulate the body’s response to this new influx of chemicals. It’s a bit like taking that first (and hopefully last!) drag on a cigarette. When you inhale, your face flushes; you feel light-headed and maybe even a bit sick to your stomach.

Scientists now know that the main sex hormones—testosterone, estrogen, and progesterone—trigger physical changes in adolescents such as a deepening of the voice and the growth of facial hair in boys and the development of breasts and the beginning of menstruation in girls. These sex hormones are present in both sexes throughout childhood. With the onset of puberty, however, the concentrations of these chemicals change dramatically. In girls, estrogen and progesterone will fluctuate with the menstrual cycle. Because both hormones are linked to chemicals in the brain that control mood, a happy, laughing fourteen-year-old can have an emotional meltdown in the time it takes her to close her bedroom door. With boys, testosterone finds particularly friendly receptors in the amygdala, the structure in the brain that controls the fight-or-flight response—that is, aggression or fear. Before leaving adolescence behind, a boy can have thirty times as much testosterone in his body as he had before puberty began.

Sex hormones are particularly active in the limbic system, which is the emotional center of the brain. That explains in part why adolescents not only are emotionally volatile but may even seek out emotionally charged experiences—everything from a book that makes her sob to a roller coaster that makes him scream. This double whammy—a jacked-up, stimulus-seeking brain not yet fully capable of making mature decisions—hits teens pretty hard, and the consequences to them, and their families, can sometimes be catastrophic.

While scientists have long known how hormones work, only in the past five years have they been able to figure out why they work the way they do. Because sex hormones are present at birth, they essentially hibernate for more than a decade. What, then, triggers them to begin puberty? A few years ago, researchers discovered that puberty (#litres_trial_promo) is initiated by what appears to be a game of hormonal dominoes, which begins with a gene producing a single protein, named kisspeptin, in the hypothalamus, the part of the brain that regulates metabolism. When that protein connects with, or “kisses,” receptors on another gene, it eventually triggers the pituitary gland to release its storage of hormones. Those surges of testosterone, estrogen, and progesterone in turn activate the testes and ovaries.

After sex hormones were discovered, for the rest of the twentieth century they became the dominant theory of, and favorite explanation for, adolescent behavior. The problem with this theory is that teenagers don’t have higher hormone levels than young adults—they just react differently to hormones. For instance, adolescence is a time of increased response (#litres_trial_promo) to stress, which may in part be why anxiety disorders, including panic disorder, typically arise during puberty. Teens simply don’t have the same tolerance for stress that we see in adults. Teens are much more likely to exhibit stress-induced illnesses and physical problems, such as colds, headaches, and upset stomachs. There is also an epidemic of symptoms ranging from nail biting to eating disorders that are commonplace in today’s teens. We have a tsunami of input coming at teens from home, school, peers, and, last but not least, the media and Internet that is unprecedented in the history of mankind. Why are adults less susceptible to the effect of all this stimulation? In 2007, researchers at the State University of New York (SUNY) Downstate Medical Center reported that the hormone tetrahydropregnanolone (THP), usually released in response to stress to modulate anxiety, has a reverse effect in adolescents, raising anxiety instead of tamping it down. In an adult, this stress hormone acts like a tranquilizer in the brain and produces a calming effect about a half hour after the anxiety-producing event. In adolescent mice, THP is ineffective in inhibiting anxiety. So anxiety begets anxiety even more so in teens. There is real biology behind that.

In order to truly understand why teenagers are moody, impulsive, and bored; why they act out, talk back, and don’t pay attention; why drugs and alcohol are so dangerous for them; and why they make poor decisions about drinking, driving, sex—you name it—we have to look at their brain circuits for answers. The elevated secretion of sex hormones is the biological marker of puberty, the physiological transformation of a child into a sexually mature human being, though not yet a true “adult.”

While hormones can explain some of what is going on, there is much more at play in the teenage brain, where new connections between brain areas are being built and many chemicals, especially neurotransmitters, the brain’s “messengers,” are in flux. This is why adolescence is a time of true wonder. Because of the flexibility and growth of the brain, adolescents have a window of opportunity with an increased capacity for remarkable accomplishments. But flexibility, growth, and exuberance are a double-edged sword because an “open” and excitable brain also can be adversely affected by stress, drugs, chemical substances, and any number of changes in the environment. And because of an adolescent’s often overactive brain, those influences can result in problems dramatically more serious than they are for adults.

2 (#ulink_1145819e-fc08-5c75-9db0-5828aaf7e0ed)

Building a Brain (#ulink_1145819e-fc08-5c75-9db0-5828aaf7e0ed)

The human body is amazing, the way it neatly tucks all these complex organs into this finite space and connects them into one smoothly functioning system. Even the average human brain is said by many scientists to be the most complex object in the universe. A baby brain is not just a small adult brain, and brain growth, unlike the growth of most other organs in the body, is not simply a process of getting larger. The brain changes as it grows, going through special stages that take advantage of the childhood years and the protection of the family, then, toward the end of the teen years, the surge toward independence. Childhood and teen brains are “impressionable,” and for good reason, too. Just as baby chicks can imprint on the mother hen, human children and teens can “imprint” on experiences they have, and these can influence what they choose to do as adults.

Such was the case with me. I “imprinted” on neuroscience and medicine pretty early on. My experiences cultivated in me a curiosity that I found irresistible, sustaining me from my high school years through medical school and graduate research, and to this very day. I grew up the oldest of three children in a comfortable family home in Connecticut, just forty minutes from Manhattan. I happened to live in Greenwich, which even back then was the home of actors, authors, musicians, politicians, bankers, and the independently wealthy. The actress Glenn Close was born there, President George H. W. Bush grew up there, and the great bandleader Tommy Dorsey died there.

My parents were from England; they had immigrated after World War II, and my dad came over after medical school in London to do his urological surgery residency at Columbia. To them, Greenwich seemed a great place to settle within commuting distance of New York City. It was a matter of convenience, and they were pretty oblivious to the celebrity status of the town. Perhaps because of my father, I was open-minded about learning math and science. For me a major “imprinting” moment that propelled me in the direction of medicine was a ninth-grade biology class at Greenwich Academy. The best part to me, memorable in fact, was when we each got a fetal pig to dissect. While many of my classmates slumped in their seats at the proposition of slicing up these small mammals, some rushing to the girls’ washrooms with waves of nausea, a few of us jumped into the task at hand. It was one of those defining moments. The scientists had separated from those destined to be the writers, lawyers, and businesspeople of the future.

Injected with latex, the pigs’ veins and arteries visibly popped out with their colorful hues of blue and red. I’m a very visual person; I also like thinking in three dimensions. That visual-spatial ability comes in handy with neurology and neuroscience. The brain is a three-dimensional structure with connections between brain areas going in every direction. It helps to be able to mentally map these connections when one is trying to determine where a stroke or brain injury is located in a patient presenting with a combination of neurological problems—definitely a plus for a neurologist. Actually, that’s how the minds of most neurologists and neuroscientists work. We’re a breed that tends to love to look for patterns in things. I’ve never met a jigsaw puzzle, in fact, that I didn’t like. My attraction to neuroscience in high school and college began at a time before CT scans and MRIs, when a doctor had to imagine where the problem was inside the brain of a patient by picturing the organ three-dimensionally. I’m good at that. I like being a neurological detective, and as far as I’m concerned, neuroscience and neurology turned out to be the perfect profession for me to make use of those visuospatial skills.

If the human brain is very much a puzzle, then the teenage brain is a puzzle awaiting completion. Being able to see where those brain pieces fit is part of my job as a neurologist, and I decided to apply this to a better understanding of the teen brain. That’s also why I’m writing this book: to help you understand not only what the teen brain is but also what it is not, and what it is still in the process of becoming. Among all the organs of the human body, the brain is the most incomplete structure at birth, just about 40 percent the size it will be in adulthood. Size is not the only thing that changes; all the internal wiring changes during development. Brain growth, it turns out, takes a lot of time.

And yet the brain of an adolescent is nothing short of a paradox. It has an overabundance of gray matter (the neurons that form the basic building blocks of the brain) and an undersupply of white matter (the connective wiring that helps information flow efficiently from one part of the brain to the other)—which is why the teenage brain is almost like a brand-new Ferrari: it’s primed and pumped, but it hasn’t been road tested yet. In other words, it’s all revved up but doesn’t quite know where to go. This paradox has led to a kind of cultural mixed message. We assume when someone looks like an adult that he or she must be one mentally as well. Adolescent boys shave and teenage girls can get pregnant, and yet neurologically neither one has a brain ready for prime time: the adult world.

The brain was essentially built by nature from the ground up: from the cellar to the attic, from back to front. Remarkably, the brain also wires itself starting in the back with the structures that mediate our interaction with the environment and regulate our sensory processes—vision, hearing, balance, touch, and sense of space. These mediating brain structures include the cerebellum, which aids balance and coordination; the thalamus, which is the relay station for sensory signals; and the hypothalamus, a central command center for the maintenance of body functions, including hunger, thirst, sex, and aggression.

I have to admit that the brain is not very exciting to look at. Sitting atop the spinal cord, it is light gray in color (hence the term “gray matter”) and has a consistency somewhere between overcooked pasta and Jell-O. At three pounds, this wet, wrinkled tissue is about the size of two fists held next to each other and weighs no more than a large acorn squash. The “gray matter” houses most of the principal brain cells, called neurons: these are the cells responsible for thought, perception, motion, and control of bodily functions. These cells also need to connect to one another, as well as to the spinal cord, for the brain to control our bodies, behavior, thoughts, and emotions. Neurons send most of their connections to other neurons through the “white matter” in the brain. The commonly used brain imaging tool, magnetic resonance imaging, or MRI, shows the distinction between gray and white matter beautifully. On the outside surface, the brain has a rippled structure. The valleys or creases are referred to as sulci and the hills are referred to as gyri. Figure 1 (#litres_trial_promo) shows an image from a brain’s MRI scan, like those done on patients. There are two sides to the brain, each called a hemisphere. (When an MRI image shows a cut across the middle in one direction or the other [slice angles A and B], it is easier to see the two sides.) The most superficial layer of the brain is called the cortex and it is made up of the gray matter closest to the surface, with the white matter located beneath it. The gray matter is where most of the brain cells (neurons) are located. The neurons connect directly to those close by, but in order to connect to neurons in other parts of the brain, in the other hemisphere, or in the spinal cord to activate muscles and nerves in our face or body, the neurons send processes down through the white matter. The white matter is called “white” because in real life and also in the MRI scans its color is light, owing to the fact that the neuron processes running through here are coated with a fatty insulator-like substance called myelin, which truly is white in color.

As I said before, sheer size—or even weight, for that matter—doesn’t mean everything. A whale brain weighs about twenty-two pounds; an elephant brain about eleven. If intellect were determined by the ratio of brain weight to body weight, we’d be losers. Dwarf monkeys have one gram of brain matter for every twenty-seven grams of body matter, and yet the ratio for humans is one gram of brain weight to forty-four grams of body weight. So we actually have less brain per gram of body weight than some of our primate cousins. It is the complexity of the way neurons are hooked up to one another that matters. Another example of how little the weight of the brain has to do with its functioning, at least in terms of intelligence, is that the human female brain is physically smaller in size than the male brain but IQ ranges are the same for the two sexes. At only 2.71 pounds, the brain of Albert Einstein (#litres_trial_promo), indisputably one of the greatest thinkers of the twentieth century, was slightly underweight. But recent studies also show that Einstein had more connections per gram of brain matter than the average person.

FIGURE 1. The Basics of Brain Structure: A magnetic resonance imaging (MRI) scan of a brain. The horizontal and vertical cross sections (slice angles A and B) show the cortex (gray matter) on the surface and the white matter underneath.

The size of the human brain does have a lot to do with the size of the human skull. Basically, the brain has to fit inside the skull. As a neurologist, you have to measure the size of children’s heads as they grow up. I have to admit there were occasions when I did this with my own sons—just like noting changes in their height—to make sure they were on track and in the normal range for skull size. When they were older, they thought I was nuts, of course, but when they were babies and toddlers, I just couldn’t resist coming at them with a tape measure I’d take from my sewing kit, then trying to get them to stop squiggling free so I could take just one more measurement. The truth is, skull size doesn’t tell us a lot. It’s a gross measurement, and the skull can be large or small for a variety of reasons. There are disorders in which the head is too big and disorders in which the head is too small. The most important characteristic of the skull is that it limits the size of the brain. Eight of the twenty-two bones in the human skull are cranial, and their chief job is to protect the brain. At birth, these cranial bones are only loosely held together with connective tissue so that the head can compress a bit as the baby moves through the birth canal. The skull bones are loosely attached and have spaces between them: one of these is the “soft spot” all babies have at birth, which closes during the first year of life as the bones fuse together. Most growth in head size occurs from birth to seven years, with the largest increase in cranial size occurring during the first year of life because of massive early brain development.

So with a fixed skull size, human evolution did its best to jam as much brain matter inside as possible. Homo erectus, from whom the modern human species evolved, appeared about two million years ago. Its brain size was only about 800 to 900 cubic centimeters, as opposed to the approximately 1,500 cubic centimeters of today’s Homo sapiens. With modern human brains nearly double the size of these ancestors’, the skull had to grow as well and, in turn, the female pelvis had to widen to accommodate the larger head. Evolution accomplished all of this within just two million years. Perhaps that’s why the brain’s design, while extraordinarily ingenious, also gives a bit of the impression that it was updated on the fly. How else to explain the cramped conditions? Like too many clothes crammed in too small a closet, the evolution-sculpted brain looks like a ribbon repeatedly folded and pressed together. These folds, with their ridges (gyri) and valleys (sulci), as seen in Figure 1 (#litres_trial_promo), give the human brain an irregular surface appearance, the result of all that tight packing inside the skull. Not surprisingly, humans have the most complex brain folding structure of all species. As you move down the phylogenic scale to simpler mammals, the folds begin to disappear. Cats and dogs have some, but not nearly as many as humans do, and rats and mice have virtually none. The smoother the surface, the simpler the brain.

While the brain looks fairly symmetrical from the outside, inside there are important side-to-side differences. No one is really sure why, but the right side of your brain controls the left side of your body and vice versa; this means that the right cortex governs the movements of your left eye, left arm, and left leg and the left cortex governs the movements of your right eye, right arm, and right leg. For vision, the input from the left side of the visual field goes through the right thalamus to the right occipital cortex, and information from the right visual field goes to the left. In general, visual and spatial perception is thought to be more on the right side of the brain.

The image of the body, in fact, can actually be “mapped” onto the surface of the brain, and this map has been termed the “homunculus” (Latin for “little man”). In the motor and sensory cortex, the different areas of the body get more or less real estate depending upon their functional importance. The face, lips, tongue, and fingertips get the largest amount of space, as the sensation and control necessary for these areas have to be more accurate than for other areas such as the middle of the back.

An early-twentieth-century Canadian neuroscientist (#litres_trial_promo), Wilder Penfield, was the first to describe the cortical map, or homunculus, which he did after doing surgery to remove parts of the brain that caused epileptic seizures. He would stimulate areas of the surface to determine which parts would be safe to remove. Stimulating one area would cause a limb or facial part, for instance, to twitch, and having done this on many patients he was able to create a standard map.

FIGURE 2. The “Homunculus”: A “map” of the brain illustrating the regions that control the different body parts.

The amount of brain area devoted to a given body part varies depending on how complicated its function is. For instance, the area given to hands and fingers, lips and mouth, is about ten times larger than that for the whole surface of the back. (But then, what do you do with your back anyway—except bend it?) This way all the brain regions for the same part of the body end up in close proximity to one another.

My undergraduate thesis at Smith College in Northampton, Massachusetts, examined several of those areas of the brain given over to individual body parts and whether overstimulation of one of the body’s limbs might result in more brain area devoted to that part. This was actually an early experiment in brain plasticity, to see if the brain changed in response to outward stimulation. Many impressive studies that have been done since the late 1970s back up the whole concept of imprinting. Some of the most famous work (#litres_trial_promo), which inspired me to do my little undergraduate thesis, was done by a pair of Harvard scientists named David Hubel and Torsten Wiesel. The term that started to be used was “plasticity,” meaning that the brain could be changed by experience—it was moldable, like plastic. Hubel and Wiesel showed that if baby kittens were reared with a patch on one eye during the equivalent of their childhood years (they looked sort of like pirate kittens!), for the rest of their lives they were unable to see out of the eye that had been patched. The scientists also saw that the brain area devoted to the patched eye had been partially taken over by the open eye’s connections. They did another set of experiments where the kittens were raised in visual environments with vertical lines and found that their brains would respond only to vertical lines when they were adults. The point is that the types of cues and stimuli that are present during brain development really change the way the brain works later in life. So my experiment in college showed basically the same thing, not for vision, but rather for touch.

I actually had some fun showing off this cool imprinting effect in our everyday lives. Our beloved cat had died at the ripe old age of nineteen, and we all missed her so. Of course, it didn’t take long before Andrew, Will, and I were at the local animal shelter, looking at kittens to bring home. We fell in love with the runt of a litter and brought home the most petite and needy little tabby kitten you could ever imagine. The boys came up with a name: Jill. Jill was always on our laps; she was a very people-friendly cat. I remembered the experiments on brain plasticity and said to Andrew and Will, when we hold her, let’s massage her paws and see if she becomes a more coordinated cat. So anytime we had her in our laps, we would massage her paws with our hands, spreading them out, touching the little “fingers” that cats’ paws contain. Sure enough, Jill started to use her paws much more than any other cat we had ever had (and I have had back-to-back cats since the age of eight). She used her paws for things most cats don’t. She was very “paw-centric,” going around the house batting small objects off tables and taking obvious pleasure in watching them hit the ground. This was a source of consternation as not all the things she knocked off were unbreakable. She also often used her left paw to eat, gingerly reaching into the cat food can with her paw and scooping up food to bring to her mouth. Watching her, we started to notice that she almost always used her left paw to do these things. We had a left-pawed cat! Then suddenly we realized that when we picked her up to massage her paws, she was facing us and because we are all right-handed, we were always stimulating her left paw much more than her right! Home neuronal plasticity demonstration project accomplished. I know if we could have looked into her brain, we’d have seen that she had more brain space given over to her paws, and especially her left paw, than the average cat. This same phenomenon of reallocating brain space based on experience during life happens in people, too. We call this part of life the critical period, when “nurture,” that is, the environment, can modify “nature.” But more on that later.

So what I have just told you is that brain areas for vision and body parts are compartmentalized in different places, but that they can shrink or grow relative to one another during development based on how much the senses are used. Structurally, the human brain is divided into four lobes: frontal (top front), parietal (top back), temporal (sides), and occipital (back). The brain sits on the brainstem, which connects to the spinal cord. In the rear of the brain, the cerebellum regulates motor patterning and coordination, and the occipital lobes house the visual cortex. The parietal lobes house association areas as well as the motor and sensory cortices (which include the homunculus in Figure 2 (#litres_trial_promo)). The temporal lobes include areas involved in the regulation of emotions and sexuality. Language is also located here, more specifically in the dominant hemisphere (the left temporal lobe for right-handed people and 85 percent of left-handed people, and the right temporal lobe for that small group of truly strong lefties). The frontal lobes sit most anteriorly and this area is concerned with executive function, judgment, insight, and impulse control. Importantly, as the brain matures from back to front in the teen years the frontal lobes are the least mature and the least connected compared with the other lobes.

FIGURE 3. The Lobes of the Brain: A. The brain matures from the back to the front. B. The cortex of the brain can be divided into several main areas based on function.

The brain is divided into specialized regions for each of the senses. The area for hearing, or the auditory cortex, is in the temporal lobes; the visual cortex is in the occipital lobes; and the parietal lobes house movement and feeling in the motor and sensory cortices, respectively. Other parts of the brain have nothing to do with the senses, and the best example of this is the frontal lobes, which make up more than 40 percent of the human brain’s total volume—more than in any other animal species. The frontal lobes are the seat of our ability to generate insight, judgment, abstraction, and planning. They are the source of self-awareness and our ability to assess dangers and risk, so we use this area of the brain to choose a course of action wisely.

Hence, the frontal lobes are often said to house the “executive” function of the human brain. A chimpanzee’s frontal lobes come closest to the human’s in terms of size, but still make up only around 17 percent of its total brain volume. A dog’s frontal lobes make up just 7 percent of its brain. For other species, different brain structures are more important. Compared with humans, monkeys and chimpanzees have a much larger cerebellum, where control of physical coordination is honed. A dolphin’s auditory cortex is more advanced than a human’s, with a hearing range at least seven times that of a young adult. A dog has a billion olfactory cells in its brain compared with our measly twelve million. And the shark has special cells in its brain that help it detect electrical fields—not to navigate but to pick up electrical signals given off by the scantest of muscle movements in other fish as they try to hide from this deadly predator.

We humans don’t have a lot else going for us other than our wile and wit. Our competitive edge is our ingenuity, brains over brawn. This edge happens to take the longest time to develop, as the connectivity to and from the frontal lobes is the most complex and is the last to fully mature. This “executive function” thus develops slowly: we certainly are not born with it!

So in what order are these brain regions all connected to one another during childhood and adolescence? This could never have been learned before the advent of modern brain imaging. New forms of brain scans, called magnetic resonance imaging (MRI), not only can give us accurate pictures of the brain inside the skull but also can show us connections between different regions. Even better, a new kind of MRI, called the functional MRI, abbreviated fMRI, can actually show us what brain areas turn one another on. So we can actually see if areas that “fire” together are “wired” together. In the last decade, the National Institutes of Health conducted a major study to examine how brain regions (#litres_trial_promo) activate one another over the first twenty-one years of life.

What they found was remarkable: the connectivity of the brain slowly moves from the back of the brain to the front. The very last places to “connect” are the frontal lobes (Figure 4 (#litres_trial_promo)). In fact, the teen brain is only about 80 percent of the way to maturity. That 20 percent gap, where the wiring is thinnest, is crucial and goes a long way toward explaining why teenagers behave in such puzzling ways—their mood swings, irritability, impulsiveness, and explosiveness; their inability to focus, to follow through, and to connect with adults; and their temptations to use drugs and alcohol and to engage in other risky behavior. When we think of ourselves as civilized, intelligent adults, we really have the frontal and prefrontal parts of the cortex to thank.

Because teens are not quite firing on all cylinders when it comes to the frontal lobes, we shouldn’t be surprised by the daily stories we hear and read about tragic mistakes and accidents involving adolescents. The process is not really done by the end of the teen years—and as a result the college years are still a vulnerable period. Recently a friend of mine told me about his son’s college classmate, Dan, an all-around great kid who’d rarely caused his parents to worry. He was popular, had been a star ice hockey player in high school, and was a finance major in college. Over the summer my friend’s son got a phone call from Dan’s mother. Dan had drowned the night before, she told him. He’d been out with friends, drinking, and sometime between three and four in the morning, on their way home, the group—there were eight of them—decided they wanted to cool off, so they stopped at the local tennis club. The club was closed, of course, but the locked gate didn’t stop them. All eight scaled the fence and jumped into the pool. It was only after they’d gotten home that someone said, “Where’s Dan?” Racing back to the club, they found their friend facedown in the water. The medical examiner listed the cause of death as accidental drowning due to “acute alcohol intoxication.” One of the news reports I read made me shake my head: “Police are asking kids and adults to think twice about potential dangers before taking any risks that could turn deadly.”

FIGURE 4. Maturing Brain: The Brain “Connects” from Back to Front: A. A functional MRI (fMRI) scan can map connectivity in the brain. Darker areas indicate greater connectivity. B. Myelination of white matter tracks cortex maturation from back to front; this is why the frontal lobes are the last to be connected. C. Serial connectivity scans reveal that frontal lobe connectivity is delayed until age twenty or older.

“Think twice.”

How many times have we all said this to our teenage sons and daughters? Too many times. Still, as soon as I heard about Dan, I called my boys to tell them the story. You have to remember this, I told them. This is what happens. Drinking and swimming don’t go together. Neither does the decision to suddenly scale a fence in the middle of the night, or jump into a pool with seven friends who are also intoxicated.

How parents deal with these tragic stories and talk about them with their own kids is critical. It shouldn’t be, “Oh, wow, I’m so glad that wasn’t my child.” Or, “My teenager would never have done that.” Because you don’t know. Instead, you have to be proactive. You have to stuff their minds with real stories, real consequences, and then you have to do it again—over dinner, after soccer practice, before music lessons, and, yes, even when they complain they’ve heard it all before. You have to remind them: These things can happen anytime, and there are many different situations that can get them into trouble and that can end badly.

One of the reasons that repetition is so important lies in your teenager’s brain development. One of the frontal lobes’ executive functions includes something called prospective memory, which is the ability to hold in your mind the intention to perform a certain action at a future time—for instance, remembering to return a phone call when you get home from work. Researchers have found not only that prospective memory is very much associated with the frontal lobes but also that it continues to develop and become more efficient specifically between the ages of six and ten, and then again in the twenties. Between the ages of ten and fourteen, however, studies reveal no significant improvement. It’s as if that part of the brain—the ability to remember to do something—is simply not keeping up with the rest of a teenager’s growth and development.

The parietal lobes, located just behind the frontal lobes, contain association areas and are crucial to being able to switch between tasks, something that also matures late in the adolescent brain. Switching between tasks is nearly a constant need in today’s world of information overload, especially when you consider the fact that multitasking—doing two cognitively complex things at the same time—is actually a myth. Chewing gum and doing virtually anything else is not multitasking because chewing gum involves no real cognitive focus. Both talking on a cell phone and driving, however, do involve cognitive focus. Because there are limits to how many things the human brain can focus on at any one time, when someone is engaged in multiple cognitively significant activities, like talking and driving, the brain must constantly switch back and forth between the two tasks. And when it does, neither of those tasks is being accomplished particularly well.

The parietal lobes help the frontal lobes to focus (#litres_trial_promo), but there are limits. The human brain is so good at this juggling that it seems as though we are doing two tasks at the same time, but really we’re not. Scientists at the Swedish medical university Karolinska Institutet measured those limits in 2009 when they used fMRI images of people multitasking to model what happens in the brain when we try to do more than one thing at a time. They found that a person’s working memory is capable of retaining only between two and seven different images at any one time; this means that focusing on more than one complex task is virtually impossible. Focusing chiefly happens in the parietal lobes, which dampen extraneous activity to allow the brain to concentrate on one thing and then another.

The problem of having immature parietal lobes was illustrated in a segment on Good Morning America in May 2008 by the ABC TV correspondent David Kerley and his teenage daughter Devan. Using a course set up by Allstate Insurance, and with her father in the passenger seat, Devan, who had been driving for a year, was instructed about speed, braking, and turning and allowed to take a practice run through the course. Then she was given a series of three “distractions” to handle while navigating the course’s twists and turns. First, she was handed a BlackBerry and told to read the text on the screen while driving. She hit several cones. Next, three of her friends were put in the backseat and a lively conversation ensued. Devan hit more cones. Finally, Devan was handed a package of cookies and a bottle of water, and just passing the cookies around and holding the bottle of water caused her to run over several more cones. Multitasking is not only a myth but a dangerous one, especially when it comes to the teenage brain.

“Multitasking” has become a household word. The research in Sweden suggests that there are limits. Teenagers and young adults pride themselves on their ability to multitask. Have today’s teens and young adults imprinted on a multitasking world? Maybe. In studying how young adults these days handle distractions, researchers at the University of Minnesota have shown that the ability to successfully switch attention among multiple tasks is still developing through the teenage years. So it may not come as a surprise to learn that of the nearly six thousand adolescents who die (#litres_trial_promo) every year in automobile accidents, 87 percent die because of distracted driving.

The question of whether today’s teens and young adults have a special skill set for learning while distracted was more formally tested in 2006 by researchers at the University of Missouri. They took twenty-eight undergraduates, including kids in their late teens, and asked them to memorize lists of words and then recall these words at a later time. To test whether distraction affected their ability to memorize, the researchers asked the students to perform a concurrent task—placing a series of letters in order based on their color by pressing the keys on a computer keyboard. This task was given under two conditions: when the students were memorizing the lists of words and when the students were recalling those lists for the researchers. The Missouri scientists discovered that simultaneous tasks (#litres_trial_promo) affected both encoding (memorizing) and retrieving (recalling). When the keyboard task was given while the students were trying to recall the previously memorized words (which is akin to taking a test or exam), there was a 9 to 26 percent decline in their ability to memorize the words. The decline was even more if the concurrent distracting task occurred while they were memorizing, in which case their performance decreased by a whopping 46 to 59 percent.

These results certainly have implications for the teen bedroom during a homework night! I not-so-fondly remember walking in on my sons during evening homework time to find them with the television on, headphones attached to iPods, all the while messaging someone on the lower corner of their computer screens and texting someone else on their iPhones. It wasn’t a problem, they protested, when I suggested they concentrate on their homework, assuring me their course reviews for the next day’s exams were totally unaffected by the thirty-two other things they were doing at the same time. I didn’t buy it. So I buttressed my argument with the Missouri data. I put Figure 5 (#litres_trial_promo) in this book in case you want to use it to make the same point to your teen.

FIGURE 5. Multitasking Is Still Not Perfect in the Teen Brain: College students were tested under three conditions: No Distraction (full attention), Distracted Attention (DA) when memorizing (DA at encoding), and Distracted Attention when recalling (DA at retrieval). Students performed poorly when multitasking during recall, and even worse when they multitasked while memorizing.

Attention is only one way we can assess how the brain is working. There’s a lot more under the hood of the brain than just the four lobes, so returning to Figure 3 (#litres_trial_promo) let’s start at the back, where we find the brainstem at the very bottom of the brain, attached to the spinal cord. The brainstem controls many of our most critical biological functions, like breathing, heart rate, blood pressure, and bladder and bowel movements. The brainstem is on “automatic”—you are not even aware of what it does, and you normally don’t voluntarily control what it does. The brainstem and spinal cord are connected to the higher parts of the brain through way station areas, like the thalamus, which sits right under the cortex. Information from all the senses flows through the thalamus to the cortex. Right below the cortex are structures called the basal ganglia, which play a big role in making coordinated and patterned movements. The basal ganglia are directly affected by Parkinson’s disease and account for the trembling and the appearance of being frozen, or unable to move, which are the hallmark symptoms of Parkinson’s patients.

As we move closer to the cortex, we encounter structures that together make up what is called the limbic system. The limbic system gets involved in memories and also emotions. A part of the brain we will talk about a lot in this book is the hippocampus. The hippocampus is a little seahorse-shaped structure underneath the temporal lobe. In fact the name “hippocampus” comes from the Latin word for “horse” because of the shape. The hippocampus is truly the brain’s “workhorse” for memory processing—it is used for encoding and retrieving memories.

So what do we know about our memory workhorse? It has the highest density of excitatory synapses in the brain. It is a virtual beehive of activity, and turns on with every experience. As we will explain later, the hippocampus in the adolescent brain is relatively “supercharged” compared with an adult’s.

The connection of the hippocampus to memory (#litres_trial_promo) was recognized some six decades ago through the unforeseen consequences of one patient’s radical brain surgery. This surgery was performed in 1953 on a twenty-seven-year-old Connecticut man who, until his death several years ago, was known only by his initials, H.M. He underwent an experimental operation in an attempt to cure him of frequent and severe epileptic seizures. So incapacitating was H.M.’s epilepsy that he was unable to hold down even a factory job. When the Yale neurosurgeon William Beecher Scoville removed most of H.M.’s medial temporal lobe, which was causing his seizures, the operation appeared to be a success. By cutting away brain tissue in the area of the seizures, Scoville dramatically reduced their frequency and severity. In the process, though, he also removed a large portion of H.M.’s hippocampus. (That the hippocampus is critical for memory formation was unknown at the time; the case of H.M. shed much light on the subject.) What became clear when H.M. awoke was that while his seizures were by and large gone, so, too, was his ability to turn short-term memories into long-term memories. Essentially, H.M. could remember his past—everything before the time of the operation—but for the rest of his life he had no short-term memory and could not remember what happened to him, what he said or did or thought or felt or whom he met, in the decades following the surgery. H.M.’s loss, as often happens in the history of science, was neuroscience’s gain. For the first time researchers could point to a specific brain region (the temporal lobe) and brain structure (the hippocampus) as the seat of human memory.

Next door to the hippocampus, in another part of the limbic system under the temporal lobe, is another key brain structure, the amygdala, which is involved in sexual and emotional behavior. It is very susceptible to hormones, such as sex hormones and adrenaline. It is sort of the seat of anger, and when stimulated in animal experiments, it has been shown to produce rage-like behavior. The limbic system can be thought of as a kind of crossroads of the brain, where emotions and experiences are integrated.

A slightly unbridled and overexuberant immature amygdala is thought to contribute to adolescent explosiveness; this explains in part the hysteria that greets parents when they say no to whatever it is their adolescent thinks is a perfectly reasonable request. Cross that immature amygdala with a teen’s loosely connected frontal lobe, and you have a recipe for potential disaster. For example, the sixteen-year-old patient of a colleague of mine was so incensed when his parents said driving was a “privilege” (for which he did not yet qualify), and not a “right,” that he stole the car keys and drove away from the house. He didn’t get very far, though. He forgot the garage door was closed and plowed right through it. One of my colleagues also told me that, because he himself had three grown daughters, rather than sons, he had few “terrible teen tales” to tell. Then he reconsidered: “Oh, yes, there was the weekend we were away and the ‘couple of friends’ became a party that got out of hand, including the raid on our wine cellar, a minor fender bender with our stolen liquor in the trunk, and maybe a navel ring (which I never knew about until years later after it disappeared). But all’s well that ends well.”

3 (#ulink_3d862f50-562d-5909-94e3-077c1049aeef)

Under the Microscope (#ulink_3d862f50-562d-5909-94e3-077c1049aeef)

If you pick out any random region of brain and look at it under a microscope, you’ll find it jam-packed with cells. In fact, there is almost no space between the billions of cells in the brain. Evolution made sure of that, putting to use every cubic micron wisely. A cell is the body’s smallest unitary building block, and each has its own command center, called a nucleus, a large oval body near the center of the cell. There are more than two hundred different types of cells making up every organ, tissue, muscle, etc. A unique cell type in the brain is the neuron. This is a cell we will talk about frequently in this book. Thoughts, feelings, movements, and moods are nothing more than neurons communicating by sending electrical messages to one another.

I remember my first time looking at brain cells under a microscope. In the mid- to late 1970s the only way to study changes in neurons, for instance the changes that occur during learning, was by looking through a microscope at individual cells over a given period of time. Today, we have amazing tools—brain imaging scans and specialized microscopes—that allow us to look into the brain and see cells and synapses change in real time. If you are learning something right now, as you read this, your neurons will change in about fifteen minutes, creating more synapses and receptors. Changes start within milliseconds of learning something new, and can take place over a period of minutes and hours. When I look at brain cells under a microscope, I think of the billions of neurons that are interconnected and how we’re still trying to figure out the wiring. What we know now is that no two human brains are wired exactly the same, and experience shapes us all differently. It’s the final frontier, our own internal frontier, and we’re just now beginning to see all the patterns.

There are 100 billion neurons in the human brain and you could place about 30,000 of them on the head of a pin, but placed end to end the neurons in just one person’s cortex would stretch for 100,000 miles—enough to circle the globe four times. At birth, we have more neurons than at any other time in our life. In fact, our brains are at their densest before birth, between the third and sixth months of gestation. Dramatic pruning of much of that gray matter occurs in the last trimester and first year of life. Still, by the time a baby is born, he or she has a brain brimming with neurons. Why? An infant’s overabundance of neural cells is needed to respond to the barrage of stimuli that comes with entering into the world. In response to all those new sights, sounds, smells, and sensations, neurons branch out in the baby’s brain, creating a thick forest of neural connections. So why aren’t all babies tiny Mozarts and Einsteins? Because when we are born, only a very small percentage of that overflow of neurons is wired together. The information is going in, being absorbed by the neurons, but it doesn’t know where to go next. Like someone plunked down in the middle of a strange and bustling metropolis, the infant brain is surrounded with possibilities and yet has no map, no compass, to navigate this strange new world. “All infants are born in a state of psychedelic splendor (#litres_trial_promo) similar to an acid trip” is how Daniel Levitin, a neuroscientist at McGill University in Montreal, Canada, colorfully describes it.

A neuron responds to a stimulus with a burst of activity, called an action potential, which is actually an electrical signal that passes, in relay fashion, from the point of contact with the stimulus down the receiving limb of the neuron, called the dendrite, through the cell.

When we see the color red, smell a rose, move a muscle, or remember someone’s name, action potentials are happening.

FIGURE 6. Anatomy of Neuron, Axon, Neurotransmitter, Synapse, Dendrite, and Myelin: Signals between cells flow in one direction, from an axon to a dendritic spine, through a synapse. Axons with myelin coating transmit signals faster than those without. At the synapse, a transfer of neurotransmitter molecules binds to the synaptic receptor on the spine.

If you think of each neuron’s cell body as a point in a relay, there must be an incoming and an outgoing signal. Once the outgoing signal reaches the axonal bouton, or end point, it sets off a reaction causing the bouton to release packages of chemical messengers, called neurotransmitters. The point of contact between two neurons is called a synapse, and is actually a space no more than two-millionths of an inch wide. The synapse is truly where the action takes place in the brain. The signal heads down the neuron through the axon to the synapse and is then released as a chemical message. Like liquid keys, these neurotransmitters cross the synapse and lock onto the neuron on the other side, and in this way carry information from one cell to another. Once opened, the receptor causes a chain reaction of signals going down the receiving cell, triggering a pulse, or an action potential, which travels from a dendrite and through the cell body and out the axon toward another cell.

In order for neurons to survive, they need helper cells called glia. There are several types of glia: astrocytes, microglia, and oligodendrocytes. To put it simply, the astrocytes defend the neuron by helping to nourish it and cleaning up the unwanted chemicals around it. This helps keep the brain’s neurons at optimal functioning level. The microglia are tiny cells that move around the neuron and really activate when there is an infection or inflammation—they move through brain tissue to the site of action to fight these injuries, like an army-in-waiting. But because the brain is efficiently designed, microglia also have an everyday purpose, a kind of housekeeping duty, so that even when they are not activated, they are still helping maintain the health and well-being of the synapses. Oligodendrocytes are the cells that make the myelin that goes around the axon of neurons. These cells are tightly packed in the white matter, wrapping whitish-colored myelin around axons to insulate them, much like rubber around an electrical cord, allowing faster speeds of signal transmission down the axon.

While you are born with the vast majority of your neurons, most of the synapses in the cortex are not fully formed. In lower areas, like the brainstem, synapses are indeed almost fully mature. In the cortex, however, synapses are produced after birth in a burst of activity, which I mentioned earlier, known as the critical period. During this stage of development, a baby’s brain creates an astonishing two million synapses every second, allowing the infant to reach mental milestones like color vision, grasping, facial recognition, and parental attachment. It’s as if an infant’s brain is sending out billions of antennae, scanning the world for information. For each synapse to survive, it must find another neuron to send information to; this is why the number of synapses in a baby’s brain peaks in childhood. The gray matter—the brain tissue responsible for processing information—continues to thicken throughout childhood as the brain’s cells form extra connections, those limb-like dendrites. Known as arborization, this thickening is like a tree growing extra branches and roots. Stimulation, experiences, repeated sensations—all contribute to the creation of these new neural pathways. In adolescence, this “overgrowth” is responsible for a teen’s heightened capacity to learn new things quickly—everything from operating the new TV remote to speaking Mandarin Chinese. The profusion of gray matter, though, can also cause a kind of cognitive dissonance in which the brain has trouble picking out the right signals from all the “noise.” As a result, by late adolescence the brain has begun to prune away excess synapses and streamline connections.

Synapses come in two flavors: ones that excite, or turn on, the next neuron, and ones that inhibit, or turn off, the next neuron.

FIGURE 7A. Inhibitory Cells Can Stop Signaling: Inhibitory cells release inhibitory neurotransmitters onto spines, which will stop a signal in a neuron and turn the cell “off.”

FIGURE 7B. Excitatory and Inhibitory Synapses: Excitatory axons release excitatory neurotransmitters, such as glutamate, which bind to excitatory receptors and turn the neuron “on.” Inhibitory axons release inhibitory neurotransmitters, like GABA, which bind to inhibitory receptors and turn the neuron “off.”

Whether or not the synapse is excitatory or inhibitory depends upon the type of neurotransmitter the axon puts out and also on the custom-made receptor, or lock, which is the part of the synapse poised to “receive” the neurotransmitter. If you imagine the neurotransmitter as a simple geometric shape, say a square or a circle, the specific receptor for that “flavor” of neurotransmitter will have the complementary shape in order to make a perfect fit. Just as “you can’t put a square peg in a round hole,” these neurotransmitter “keys” will fit into only the perfect receptor “locks.” This helps the synapse not confuse messages. In addition to the near-perfect pairing of neurotransmitters to receptors, another way the signal is kept clean is that the astrocyte helper cells immediately clean up any leftover neurotransmitter hanging around after it gets released. This happens in milliseconds, as the timing of these signals between brain cells has to be rapid, sharp as a burst.

Once the neurotransmitter has bound and locked itself into the receptor on the receiving neuron, this pairing sets off a chain reaction. Inside the dendritic side of the synapse, there are lots of proteins that rush to work when the synapse gets excited or inhibited. The signal needs to get down the dendrite to the cell body of the neuron, where it sends a positive charge for an excitatory signal or a negative charge for an inhibitory signal. Depending on which charge is sent, the receiving neuron will get a message to either stop or start functioning. If the message is positive, the receiving neuron will send the information down its own axon and across another synaptic cleft, and so on. A neuron can have up to ten thousand synapses and can send a thousand electrical impulses every second. In one-tenth of the time it takes to blink your eyes, a single neuron can simultaneously send a signal to hundreds of thousands of other neurons.

Some of the most common excitatory neurotransmitters are epinephrine, norepinephrine, and glutamate. Inhibitory neurotransmitters, like gamma-aminobutyric acid (GABA) and serotonin, act as antianxiety nutrients, calming the body and telling it to slow down. A lack of serotonin can result in aggression and depression. Dopamine is a special neurotransmitter because it is both excitatory and inhibitory. It is also, along with epinephrine and several others, a hormone. When it acts on the adrenal glands, it is acting hormonally; when it acts in the brain, it is a neurotransmitter. As a brain chemical messenger, dopamine helps motivate, drive, and focus the brain because it is integral to the brain’s reward circuitry. It’s the “I gotta have it” neurochemical that not only reinforces goal-directed activity but also can, in certain circumstances, lead to addiction. The more dopamine that is released in the brain, the more the reward circuits are activated, and the more those circuits are activated, the bigger the craving. It doesn’t matter if the craving is at the dinner table or the card table, in the boardroom or the bedroom. For instance, scientists know that high-calorie foods produce more dopamine in the brain. Why? Because higher calories increase our chance for survival. When we crave ice cream or gambling or sex, we may not actually be craving sweets, money, or orgasms. We’re craving dopamine.

Inhibiting a neural response is just as important as activating one when it comes to “executive” brain function. Examples of things that bind to inhibitory synapses are sedatives such as barbiturates, alcohol, and antihistamines. Synapses will be critical in our discussion of the adolescent brain because both the number and the type of synapses in our brains change as we age. They also change in relation to the amount of stimulation our brains experience. One topic that will come up later is the effect of illegal and illicit drugs and alcohol on these synapses, which we will cover in the chapter on addiction.

A popular instrument used by researchers to test inhibition is the Go/No-Go task in which subjects are told to press a button (the “Go” response) when a certain letter or picture appears, and not to press it (the “No-Go” response) when the letter X appears. Several studies have shown that children and adolescents generally have the same accuracy, but the reaction times, the speed at which a subject successfully inhibits a response, dramatically decrease with age in subjects age eight to twenty. In other words, it takes longer for adolescents to figure out when not to do something.

Signals move from one area of the brain to another along fiber tracks, and some of these tracks travel down through the core regions of the brain in order to send signals to and from the spinal cord. Brains are intricately interconnected by these fibers, and research using special brain scans is rapidly evolving to look at these connections. Because axons are designed to have a rapid pulse of electricity run through them to the connection point at the synapse, they act like electrical wires conducting an electrical signal. And just as an electrical wire needs insulation in order for the electricity not to dissipate along its length, so do the axons. Since we don’t have rubber in our brains, our axons are coated with a fatty substance called myelin. (See Figure 6 (#litres_trial_promo).) The brain requires myelin in order to function normally, to get a signal from one region of the brain to another and also down to the spinal cord. As we said before, myelin is made by oligodendrocytes, and has a white hue due to its fatty content: hence the term “white matter.” By essentially “greasing” the “wires,” myelin allows signals to travel down axons faster, increasing the speed of a neural transmission as much as a hundredfold. Myelin also aids the speed of transmission by helping to cut down the synapses’ recovery time between neural firings, thereby allowing a thirtyfold increase in the frequency with which neurons transmit information. The combination of increased speed and decreased recovery time has been estimated by researchers as roughly equivalent to a three-thousand-fold increase in computer bandwidth. (Myelin also is the target of attack in the disease multiple sclerosis, or MS. Patients with MS have areas of inflammation in their white matter that come and go, and this is why they can lose functions like walking, sometimes only temporarily until the inflammation passes.)

At birth, a baby’s cortex contains little myelin; this explains why the electrical transmissions are so sluggish and an infant’s reaction times so slow. However, the baby’s brainstem is almost as fully myelinated as an adult’s, so it can control automatic functions like breathing, heartbeat, and gastrointestinal function necessary to stay alive. Connections to and from many other areas of the brain occur after birth, beginning with the motor and sensory areas at the bottom and back of the brain. As these areas become wired with myelin, infants are better able to process basic information from their senses—their eyes, ears, mouth, skin, and nose. Within the first year, the neural tracts that support brain regions involved in vision and other primary senses, as well as those involved in gross motor activity, are completed. This is, in part, why it takes about a year for a baby to become coordinated enough to walk. Much of the brain becomes insulated by age two, and high-level areas involved in language and fine motor coordination follow over the next few years when children are particularly primed to learn to talk and improve their fine motor skills. The more complex areas of the brain, especially the frontal lobes, take much, much longer and are not finished until a person is well into his or her twenties.

All of this learning is dependent on excitation, the driving force in our brains. Excitatory signals between neurons build brain connections and are required for brain development. Excitation can come from outside or inside your brain, but regardless, if a particular pathway of cells and their synapses are activated repeatedly, the synapses between them strengthen. Thus, cells that “fire” together (#litres_trial_promo) “wire” together.

In the developing brain, especially in early childhood, as groups and pathways of neurons and their synapses get activated, the process of excitation “turns on” the molecular machinery in the cell. This actually results in the building of more synapses, a process we term synaptogenesis (birth of synapses). Synapses are increased in infancy through adolescence, peaking in early childhood. Because synaptogenesis is so dependent upon brain cells being activated by one another, a child’s brain has more excitatory than inhibitory neurotransmitters and synapses compared with an adult’s brain, where there is more balance between the two.

Excitation is a key element of learning. The period in early life in which excitation is so prominent is also called the “critical period,” when learning and memory are more robust than in later life. This allows the brain to be very sensitive to excitation and grow. Unfortunately, the abundant excitation in the developing brain carries a price: the risk for overexcitation. This explains why diseases that are a result of overexcitation, like epilepsy, are more common in childhood than adulthood. Seizures are the main symptom in epilepsy, and they are caused by too many brain cells turning on together without enough inhibition to balance them.

FIGURE 8. The Young Brain Has More Excitatory Synapses Than Inhibitory Synapses: The number of synapses increases from infancy through adolescence, peaking in early childhood.

Arborization, or the branching out of neurons, peaks in the first few years of life but continues, as we’ve seen, into adolescence. Gray matter density peaks in girls at age eleven and in boys at age fourteen, and waxes and wanes throughout adolescence.

White matter, or myelin, however, has only one trajectory in adolescence: up. Jay Giedd and colleagues (#litres_trial_promo) at the National Institute of Mental Health scanned the brains of nearly one thousand healthy children, ages three to eighteen, and discovered this pattern of wiring. As we saw in Figure 4 (#litres_trial_promo), researchers at the University of California, Los Angeles, built on those findings and compared the scans of young adults, ages twenty-three to thirty, with those of teenagers, ages twelve to sixteen. They found that myelin continues to be produced well past adolescence and even into a person’s thirties, making the communication between brain areas ever more efficient.

FIGURE 9. Gender Differences in Rate of Cortical Gray Matter Growth: Like the body, the male brain is on average larger than the female brain. Rates of growth in male and female brains also are different. In females, the growth rate of two areas important for cognitive maturity—the frontal lobes and the parietal lobes—peaks in the early teen years, but in males the peak does not occur until the late teens.

Without those insulated connections, a signal from one area of the brain, say fear and stress coming from the amygdala, has trouble linking up with another part of the brain, for instance the frontal cortex’s sense of judgment. For adolescents whose brains are still being wired, this means they sometimes find themselves in dangerous situations, not knowing what they should do next. This was confirmed scientifically in a 2010 study conducted by the British Red Cross into how teenagers react to emergencies involving a friend drinking too much alcohol. More than 10 percent of all children and young teens between the ages of eleven and sixteen have had to cope at one time or another with a friend who was sick, injured, or unconscious owing to excessive alcohol consumption. Half of those had to deal with a friend who passed out. More broadly, the survey found that nine out of ten adolescents have had to deal with some kind of crisis involving another person during their teenage years—a head injury, choking, an asthma attack, an epileptic seizure, etc. Forty-four percent of the teens surveyed admitted to panicking in that emergency situation, and nearly half (46 percent) acknowledged they didn’t know how to respond to the crisis at all.

Dan Gordon, a fifteen-year-old boy (#litres_trial_promo) from Hampshire, England, who was interviewed by the Guardian for a story about the study, spoke about a house party he attended at which there was widespread underage drinking. After one girl passed out on the floor, facedown, she began to vomit, and the others in the room, all teenagers, panicked. Thinking only that they needed to prevent her from choking, they stood her up and, with effort, walked her outside for fresh air and waited for her to wake up. Dan admitted to the reporter that neither he nor anyone else at the party had thought to call for an ambulance. In other words, the teenagers’ amygdalae had signaled danger, but their frontal lobes didn’t respond. Instead, the teens acted in the moment.

My son Andrew witnessed something similar during college. He was visiting his then-girlfriend at a college in Boston. The girlfriend’s roommate also had an out-of-town visitor, a shy freshman girl from the South who quickly became intoxicated at a party in another student’s room. When Andrew and his girlfriend returned to her dorm, they found the young girl passed out, and just as in Dan Gordon’s story, they all panicked. Instead of calling 911 or campus security, or driving her to an emergency room, they found a couple of friends to help, and then drove all the way out to our house, about ten miles away.

“We didn’t want to call campus security,” Andrew’s girlfriend explained, as I observed the young girl, whom they had helped into the house and who was now almost unresponsive. “She’s a freshman. If we brought her to the health center, me and my roommate could get in trouble.”

Andrew and his former girlfriend were both twenty-one at the time, but the visiting student was just eighteen.

“What about taking her to the hospital?” I said.

“We didn’t know how drunk she was,” the other friend said. “She was talking when we put her in the car, and now she’s completely out of it.”

None of them in fact knew the girl—they had met her briefly for the first time earlier that day, when she had arrived to visit the roommate. She had her wallet and an ID from her South Carolina college with her, but no other information. The roommate who had invited her to Boston was nowhere to be found. Already drowsy, she was rapidly becoming more sedated, and then she vomited on the floor. At that point, I insisted they get her to a local community hospital just a mile from our house. It took three of them to half-carry her back to the car. About fifteen minutes later, I got a call from Andrew’s girlfriend, who said the hospital was going to admit the girl for observation. The poor thing spent an unhappy night in the hospital, and the college crew picked her up the next afternoon. On their way back to Boston, they stopped by my house to gather things they had left there the night before. The young freshman looked pale and very tired, but otherwise was fine. Apparently her blood alcohol level had peaked at 0.34, which was more than four times the legal driving limit, and life threatening. Had she not been taken to the hospital, where her stomach was pumped and charcoal administered to prevent her body from absorbing any more alcohol, I shudder to think of what might have happened. As I had a captive audience, I sat them all down in the kitchen, turned on my laptop, and showed them a chart about blood alcohol levels and the effects on coordination and consciousness. I pointed out that 0.4, which was only a little more than her blood alcohol reached at its height, can be lethal. Turns out she had done about seventeen Jell-O shots that evening—to the best of her memory. There was no point in asking the usual question—“What were you thinking?”—but I felt this was a good teaching moment to show them all how close she had come to a very different end the night before.