Unbroken Brain: A Revolutionary New Way of Understanding Addiction

by Maia Szalavitz

The same overall findings held true in Robert Sapolsky’s studies of baboons. Baboons are social primates that have a strict hierarchy but do not have access to alcohol, drugs, junk food, or cigarettes. Nonetheless, top baboons have lower “bad” cholesterol, lower blood pressure, and better functioning immune systems—and again, the lower-ranked animals are at greater risk for all types of early death. Stress linked to low status harms health by raising blood pressure and cholesterol and altering immune response—all of which affect risk for all types of disease. High levels of stress hormones can also damage certain brain cells, which increases risk of depression and probably other mental illnesses as well.

social connections themselves can actually mitigate the effects of low socioeconomic status: if you have a strong social network, no matter how poor you are, the negative effects of stress are reduced.

It’s important to note here that not all stress is bad—indeed, a small to moderate amount of stress is necessary for learning because it differentiates novel experiences from familiar ones. Stress is only bad if it is overwhelming and makes you feel helpless,

One main pathway to these changes is seen in the link between depression and status stress. First, studies find that depression is especially strongly linked to high levels of stress hormones. In the brain, high levels of these hormones can result in an excess of the neurotransmitter glutamate, which is particularly damaging to brain cells in a region important for memory and emotion called the hippocampus.

Depression tends to shrink this region; all long-lasting effective methods of treating depression, from electroconvulsive therapy (ECT) to medications (and, presumably, talk therapy, though this can’t be studied in rats and we can’t cut open human brains to check), lead to improved neural growth in the area. Severe stress in children, in fact, is more likely to lead to depression or other diagnoses than it is to cause diagnosable PTSD.

Psychologists have long observed that depressive behavior in humans looks a lot like submission behavior in other animals.

Physically, depressed people shrink back—just like low-ranked animals. They tend to be timid and compliant, lacking energy and drive.

Studies consistently find links between low socioeconomic status in humans and depression, with rates doubled among those at the bottom. (Although of course depression could also lead to unemployment and, therefore, low socioeconomic status, studies that follow children over time find that poverty tends to precede depression, rather than depression tending to cause poverty.)

between birth and the end of kindergarten, the brain has already grown to a stunning 95% of its adult size.

from puberty until around age 25, the brain undergoes a remodeling that is almost as extensive as the period of rapid change in the first 5 years.

Importantly, both adolescence and infancy are marked not only by growth but also by “pruning”—a selective reduction in both the number of connections between cells and in the number of cells themselves.

During early childhood, the brain grows billions of connections and then prunes away nearly half of them, with the timing and proportion of cells pruned dependent on the region.

In adolescence, gray matter, which is made up of the cell bodies of neurons themselves, actually shrinks significantly, most notably in the prefrontal cortex, which does not complete its development until around 25. (Incidentally, this healthy shrinkage needs to be kept in mind when evaluating studies of drugs and the teen brain: smaller or shrinking structures aren’t always a sign of pathology, but are sometimes a sign of efficiency.)

Meanwhile, new “insulation,” or myelin, also grows on the nerves that connect increasing numbers of circuits, maximizing their speed and refining other signaling qualities. This...

One of the most consistent findings in autism, for example, is early brain overgrowth, with some regions being “hyperconnected” or simply having too many cells and too many links between them.

brains work best when their connections are optimized. Too many cells or connections can cause nearly as many problems as too few, and miswired links to the wrong places can curtail communication and signaling.

most of the brain’s basic circuitry, for functions like seeing, hearing, and moving, has already been fine-tuned by puberty. What remains to be calibrated are the motivational systems, which sit mainly in the center of the brain and must be prepared to face the challenge of finding a mate and reproduction.

As neuroscientist Robert Sapolsky put it, in the teen brain, the systems that drive a desire to take on the world are “already going at full speed, while the frontal cortex is still trying to make sense of the assembly instructions.”

The systems that underlie motivation—dependent primarily on the neurotransmitter dopamine in a particular circuit in the midbrain—play a nasty trick on prepubescent kids. A change in dopamine levels draws them away from home and routine and makes the new, exciting, and dangerous seem incredibly alluring.

As the dopamine circuits rewire themselves, the previously reliable pleasures of childhood play start to grow old. What you love becomes boring and loses its flavor. Sugar itself tastes less sweet and feels less fun. (This may be why candy somehow never tastes as good as it did when you were a kid.)

While these reward regions are maturing, the process makes pleasure both more attractive and harder to get. This is because during adolescence, new experiences may spur a much bi...

if you merely offer a paltry pleasure, it may not be seen as rewarding at all to a teenager. In fact, the teen brain responds to a small reward as though it’s an insult or a punishment, which may explain some of the ingratitude and sarcasm teens display when adults praise them, feed them, and ferry them around to their activities.

A motivational system that is prone to boredom and places such high value on big rewards is bound to prompt at least some hair-raising behavior.

Teens need to become more independent and to learn to manage the risks that are present in their environment; they can’t do this without getting out there and learning by experience. Keeping them completely sheltered from risk and choice doesn’t help: brain development is “experience dependent,” meaning that it requires particular input at the right time in order to proceed appropriately.

Locking kids up “till their brains are grown” will simply either delay or distort maturation. Of course, this doesn’t mean that letting adolescents go wild is a good idea either—merely that some degree of adolescent risk taking seems to be a necessary part of normal human development.

A brain can be either highly responsive or packed with knowledge: expertise comes at the cost of flexibility, to some extent. Openness to learning is also openness to risk, for better or worse. And this means that a brain primed for learning is also a brain primed for addiction.

The real connections between dopamine and pleasure, desire, and memory show how learning actually shapes addiction and why addiction is, in fact, a learning disorder. To understand this process, we need to explore how pleasure came to be understood in the brain and what dopamine has to do with it.

The connections between dopamine in addiction and dopamine in Parkinson’s may have profound implications for the relationship between mind and brain. They suggest that dopamine may be required for the fundamental expression of drives and desires—in other words, free will.

Neurologist Oliver Sacks was among the first to explore the philosophical and psychological implications of this aspect of dopamine, connecting it to will and willingness in his 1973 account of patients with a severe form of Parkinson’s caused by a 1920s encephalitis outbreak.

Parkinson’s patients can also have the opposite problem, which is difficulty initiating or sustaining motion—or even desire to move. Before the development of L-DOPA, a precursor to dopamine that can help patients with Parkinson’s recover some function, many of the people Sacks treated had found themselves literally frozen in particular positions, unable to move without assistance for years. This paralysis is consistent with a very low level of available dopamine. By reducing the availability of dopamine in the brain, Parkinson’s can, frighteningly, affect not only what its victims are able to physically do but also what they are psychologically able to want or will.

dopamine is involved not only in movement but also in the will or even the desire to move.

Although it’s possible that dopamine in motor regions signals will or intention, and in other circuits it signifies pleasure, there is actually a simpler explanation, which also illuminates addiction.

there are at least two distinct varieties of pleasure, which are chemically and psychologically quite different in terms of their effects on motivation. These types were originally characterized by psychiatrist Donald Klein as the “pleasures of the hunt” and the “pleasures of the feast.”

As the phrase suggests, the pleasures of the hunt are the thrill of the chase: excitement, desire, stimulation, intent, a sense of power and confidence in being able to seek and get what you want. In contrast, the pleasures of the feast are those of satisfaction, comfort, relaxation, attainment, and sedation. Put another way: the pleasures of the hunt are those of lust and sexual longing and the pleasures of the feast are orgasm and afterglow.

The University of Michigan’s Kent Berridge and Terry Robinson discovered that dopamine is primarily involved in just one of these pleasures.

In Berridge and Robinson’s view, pleasure is divided into “wanting” (hunt) and “liking” (feast). As we’ll see, the distinction is especially important in addiction because each type has a different influence on learning.

At the time that they did this experiment, Berridge and his colleagues thought that dopamine was necessary for any type of pleasure. They agreed with Wise, whose view had become the conventional wisdom. So, they expected that the rats wouldn’t be able to enjoy their meals: if dopamine was required for pleasure, the animals shouldn’t be capable of liking even the most sumptuous food, since they had virtually no dopamine. Without dopamine, they shouldn’t like or be pleased by anything, in fact.

That was not the case, however. Thankfully for people who have Parkinson’s or must contend with side effects of dopamine-blocking drugs, even having extremely low levels of dopamine in the nucleus accumbens doesn’t eliminate all types of positive emotion. The rats may not have wanted their food, but when they got it, they still liked it.

While dopamine is involved in motivation or the pleasures of the hunt, that’s not the only way we can feel good. Dopamine is not necessary, it seems, for enjoying sweetness, comfort, satiation, and calmness—research suggests that these pleasures are more strongly linked to the brain’s natural opioids, or heroin-like chemicals, instead of to dopamine. And this has implications for the broader understanding of addiction.

Pharmacological Calvinism means that there’s no free lunch: using up extra dopamine today by taking drugs will require payback in low mood tomorrow. The bliss of drinking will be followed by the hammering of the hangover. In this view, unearned pleasure is actually impossible in the long run. Any high will be balanced by some type of low. Berridge and Robinson’s research, however, suggests that the reality is somewhat more complex.

The theory these scientists developed to resolve this problem—known as the “incentive salience” model—also explains an infuriating aspect of stimulant drug problems that simply isn’t captured by other theories.

Their argument is that dopamine produces desire, not satisfaction—“wanting” but not “liking.” In this view, elevating dopamine with drugs like cocaine leads to escalating desire—not escalating pleasure.

As anyone who has ever suffered from sexual frustration knows, only desire that is likely to be sated is enjoyable. If satisfaction is not likely to be forthcoming, that very same yearning can become agonizing, not at all fun. You can wind up wanting more and more of something (or someone) that you like less and less.

effect in his addiction memoir this way: “I kept pumping [cocaine] into my vein, this non-sterile solution, until my reeling consciousness, nausea, racing heart, and bloated capillaries told me that death was near. Later that night, I begged myself to stop.… But the urge would not relent.”

Sensitization and tolerance are part of the way the brain tags situations as safe and inviting or fearful and threatening.

if everything always seemed new and exciting and we didn’t habituate to it, the world would be overwhelming and we wouldn’t be able to focus on what’s genuinely changing. Without sensitization, on the other hand, our attention wouldn’t be turned toward the experiences that are real threats and we wouldn’t be able to respond to them effectively.

Addiction is a learning disorder in part because of the way it affects both the habituation and sensitization processes and also skews them.

The most important addictive learning pattern—technically known as intermittent reinforcement—was discovered by Skinner himself, in a classic case of scientific serendipity. In 1956, the behaviorist pioneer was studying learning in rats. One weekend, he realized he was running low on the food pellets he used to reward the rodents when they had learned to press levers correctly. Since he had to make these rat treats himself and he didn’t want to interrupt the experiment to make more, he decided to give the animals their rewards less frequently to stretch out what remained of his supply. To his surprise, rather than reducing the odds that the rodents would press the lever, this variable reinforcement actually made them respond more.

Later studies found that the most effective schedule of reinforcement to hook animals on a behavior pattern was the most unpredictable:

A pattern-seeking brain is prone to getting fooled by random rewards that only appear linked with behavior; attempting to find structure in intermittent reinforcement can get us stuck looking for an order that doesn’t exist. In fact, like many compulsive gamblers, Skinner’s first intermittently reinforced pigeons even developed “superstitions”—behaviors like spinning around or other particular motions that they associated with times when food rewards had actually been delivered. These actions didn’t make the random rewards any more likely, of course—but like a gambler’s lucky charm, they probably gave the animals a sense that they could affect the outcome, even though it was an illusory one.

The cynical part of me asks if this is view impacts our understanding of prayer