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Scattered Minds, The Origins and Healing of Attention Deficit DisorderGabor Maté, M.D


Scattered Minds, The Origins and Healing of Attention Deficit Disorder, Gabor Maté, M.D.

A holistic account of ADD.

“Medicine,” the Austrian philosopher Ivan Illich wrote, “tells us as much about the meaningful performance of healing, suffering, and dying as chemical analysis tells us about the aesthetic value of pottery.”
The book Scattered Minds opens with that quote, and it’s a good place to start.
Attention deficit disorder – we’ll refer to it as ADD from here on – is a poorly understood condition, author Gabor Maté argues. It’s underappreciated, often misdiagnosed, and frequently overtreated. The real problem, though, is that we tend to spend so much time analyzing chemical minutiae that we lose sight of the bigger picture.
Biochemicals in the brain do play a role in ADD, but the disorder can’t be reduced to the circulation of hormones and neurotransmitters. Nor does genetics provide a full account of ADD. As we’ll see, there is an inherited predisposition to ADD, just as there is to every other mental health disorder. But that doesn’t mean the disorder is biologically predetermined. Predispositions must be “triggered” or “activated.”
And if we want to understand how and why that happens, we have to look at the interaction of biological and environmental factors. In other words, we have to look at the development of children within families and societies.
ADD has three defining traits.
Let’s start at the beginning. What exactly is ADD?
Well, the disorder has three major traits: poor attention skills, deficient impulse control, and hyperactivity. We’ll go through each of these traits in turn, starting with poor attention skills.
What we mean here is an automatic “tuning out.” The mind is absent when its attention is required to complete tasks or process instructions. Inattentiveness takes many forms. A person with ADD might ask someone a question and zone out as they begin answering it. They might look up from a book and suddenly realize they can’t recall a single word they’ve read. Or they might enter a room and discover that they have no idea what they wanted to do in it.
Whatever its form, inattentiveness causes considerable practical hardships. Kids who can’t focus fall behind in school; adults with the same issue make silly mistakes at work and miss out on promotions. Young or old, people with ADD are constantly being chastised for failing to do things they forgot about the moment they agreed to do them.
Inattentiveness also interferes with people’s enjoyment of life. One patient told the author she had never understood music – it was a confusing, impenetrable wall of white sound. Another patient talked about how his ADD had isolated him socially. He said he felt like a human giraffe: his body lived in the same world as other people but it was as though his head was stuck in the clouds far above.
Inattentiveness is rarely total, though. In fact, doctors sometimes miss ADD diagnoses because their patients are capable of hyperattentive focus. For example, a child who is inattentive at school may happily spend hours poring over maps in the evening. The thing is, the ADD mind can muster enough focus and motivation to complete tasks if those tasks are intrinsically interesting. A child with ADD who finds geography fascinating will have no problems focusing on studying maps. But that focus doesn’t carry over to other tasks that don’t interest her – science class, say, or tidying her room. Also, hyper-attentiveness often involves shutting out the rest of the world to engage in a single absorbing activity. That, too, is a feature of poor attention regulation.
The second characteristic of ADD is impulsiveness. Poor impulse control also takes different forms. A child with ADD may speak before thinking, blurting out thoughts that others find rude or inappropriate. Or they may find it impossible to stop themselves from interrupting others. Adults with ADD are often impulse buyers. One man who the author diagnosed with ADD said he would impulse buy the entire world if he had the money. More generally, impulsiveness is often the cause of excessive risk-taking. Kids with ADD may jump off roofs on a whim; teens might binge drink alcohol they find in the kitchen cabinets for the same reason. An adult with ADD may drive recklessly fast for no other reason than she felt like it. As one of the author’s patients put it, the only thing that ever slowed her down was the siren of a police car.
The third and final trait of ADD is hyperactivity. Unlike the previous two traits, hyperactivity isn’t ubiquitous. Yes, many people with ADD can’t sit still – they fidget, drum their fingers, chew their nails, tap their feet, or can’t stop talking. But often, it’s entirely absent. Many girls with ADD, for instance, frequently go undiagnosed because their behavior isn’t a source of disturbance in classrooms: they sit still and appear to be listening to what their teachers are saying. The problem only comes to light much later when baffled parents start wondering why their well-behaved daughters are doing so poorly in school.
Some people with ADD display all three traits. In that case, they may be diagnosed with ADHD – attention deficit hyperactivity disorder. But the presence of any two of these three traits is sufficient for a physician or psychologist to diagnose ADD.
Now that we’ve defined the disorder, we can turn to its origins. What, in other words, “causes” ADD?
Stress can inhibit brain development and cause tuning out.
The consensus view is that ADD is an inherited genetic disorder. We’ll come back to that. First, though, let’s take a look at what’s happening inside the ADD brain.
Brain imaging studies show that the part of the brain which controls decision-making – the prefrontal cortex – is underactive. Or rather, it functions normally when the brain is at rest but slows down when it’s called upon to engage in tasks. Tests measuring electrical activity show that fast-wave brain activity in kids with ADD declines when they’re presented with math problems. Fast-wave activity indicates that the brain is active and engaged, and there’s an uptick in such activity in children who don’t have ADD when faced with the same problems.
The mechanism in play here has to do with the production of the neurochemical that regulates focus, attention, and motivation – dopamine. Simply put, the ADD brain doesn’t produce enough dopamine. The standard treatment for the disorder is to stimulate dopamine production in the prefrontal cortex. That’s what psychostimulants like Ritalin and Dexedrine do. They boost dopamine levels and encourage fast-wave brain activity.
These medications work, too. They increase patients’ focus and calm them down. So it looks like pharmacological interventions are ironing out a biological kink. The ADD brain, the thinking goes, is miswired – and psychostimulants compensate for this genetic deficit.
This theory isn’t exactly wrong – there is an inherited component to ADD. But the gene-centric account of the disorder obscures as much as it reveals. To explain why that is, we need to take a brief detour and look at the development of the human brain.
Let’s start with horses, though. An infant horse can run on the first day of its life. Like other young mammals, it is capable of extraordinary feats of neuro-physiological coordination at birth. The brain of a human infant, by contrast, has to develop for two years before the child can walk. Evolution was selected for larger brains in humans compared to other mammals. We can’t get into why here, so let’s just note that human brains quadrupled in size since our species last shared a common ancestor with chimpanzees a million years ago. The upshot: our brains are premature at birth. They have to be. If they weren’t, our heads would be too large to pass through the birth canal. If we weren’t born at nine months, we wouldn’t be born at all.
This means that the lion’s share of cognitive development occurs after birth. The human infant’s brain makes millions of new connections every second in her first years of life. This development is physically striking. By the age of three, an infant’s body is less than 20 percent of its adult size, but her brain is 80 percent of its adult size. The point, though, is that this development takes place in this world, among other things and other people.
There is a genetic component to this development, but it isn’t genetically predetermined. Genes are blueprints. They’re plans for how the proteins which regulate the structure and function of cells get synthesized. But plans contain potential. How that potential is expressed is a question of circumstance. Take the neurological circuitry involved in sight. The plans for this circuitry are encoded in genetic material. But the development of eyesight depends on environmental factors. If an infant who is genetically capable of developing perfectly good eyesight spends his first five years in a dark room, he’ll be blind for life. Without the input of lightwaves, this visual circuitry atrophies and dies, leaving his genetic potential unexpressed.
At this point, we can return to ADD. Focus, attention, and impulse control are also part of a complex neurological circuit located in the prefrontal cortex. No one is born with, say, fully developed impulse control, so this circuit must develop after birth. But can we identify environmental inputs which affect its development, too?
In a word, yes. Dopamine-rich nerve terminals and receptors develop in an infant’s early years. They are stimulated by joyful interactions with caregivers. Holding the loving gaze of a mother is a good example of this kind of interaction. At this moment, the infant’s brain is flooded with chemicals that promote the development of dopamine receptors in the prefrontal cortex. But what if this input is absent – what if this infant spends her early life in an emotional black box?
Studies with monkeys tell us what happens to developing brains when you physically remove caregivers. Separate an infant monkey from its mother for six days, for example, and its dopamine levels will plummet. Research with human infants tells us what happens when caregivers are emotionally absent – physically present but emotionally unavailable. One cause of such unavailability is depression. Several studies show that infants whose mothers are depressed have significantly higher cortisol levels than infants whose mothers aren’t. That’s significant because prolonged exposure to high levels of cortisol depletes dopamine.
The environmental input we’ve identified is called attunement. In the language of psychology, attunement refers to the emotional alignment of the infant and caregiver. Attunement is what happens when a mother picks up a crying baby and scrunches her face into a mask of sadness. Her facial expression doesn’t just acknowledge the baby’s sadness – it communicates that she shares that sadness. For an infant, attunement is an ecstatic experience of safety and sharing the world with another person. These dopamine-boosting interactions play a key role in the human brain’s early development.
So what happens when an infant doesn’t experience attunement? Well, she isn’t reassured; she doesn’t feel safe. She feels alone in a chaotic and menacing world. She’s stressed. And she can’t change her situation, either – her premature brain isn’t capable of mounting a fight-or-flight response. All she can do is fall back on the nature-given defense mechanism which prevents stress from becoming overwhelming and life-threatening: she stops processing stressful environmental stimuli. Her brain slows down. She tunes out.
Rising ADD rates are the result of a social crisis that affects parenting.
Environmental inputs play a key role in the development of ADD. But we also said that there’s an inherited genetic component to the disorder. How do these factors interact?
We can start answering that question by clearing up a common misconception – that there’s a specific gene coding for ADD. There isn’t. There are genes associated with ADD just as there are genes associated with depression or alcoholism. Establishing causation is trickier. Some people with this coding develop ADD, and some don’t. All we can really say is that genes are a risk factor. Studies show, for example, that children of ADD parents have an increased statistical risk of developing ADD. But the disorder is also more common in people whose parents suffer from depression, anxiety, addiction, and obsessive-compulsive disorder. There’s a link between ADD and parents struggling with dysfunction, but there isn’t an “ADD gene” to explain it.
So what does? One answer is hypersensitivity.
Some people are hyperreactive – they have intense responses to relatively negligible stimuli. When these stimuli are physical, we say they are allergic. A non-allergic person develops an irritating welt if they’re stung by a bee; an allergic person experiences a sudden drop in blood pressure and a life-threatening constriction of their airways. But the bee sting didn’t “cause” this reaction. Instead, it was the interaction between the stimulus and the person’s physiological response that brought them close to death.
When people are hyperreactive to all kinds of environmental stimuli, we call them hypersensitive. We know that people with ADD are more likely to be physiologically sensitive than the rest of the population. Children with the disorder have more allergies. They have histories of frequent colds and infections. They’re more likely to be asthmatic or have eczema. But they are also more likely to be hypersensitive to emotional stimuli.
Think of it this way. When someone scalds, say, their arm with hot water, they destroy part of the epidermis. Their skin isn’t as “thick” as it would usually be. As a result, their nerve endings are closer to the surface. Now, a stimulus as mild as a slight gust of wind is enough to cause discomfort or pain. Psychologically hypersensitive people, by analogy, are also “thin-skinned.” The nerve endings that send emotional stimuli to the brain are too close to the surface. Like the exposed nerve endings in scalded skin, they are easily irritated. Stimuli that another person might find negligible cause the person with ADD acute discomfort or pain.
Hypersensitivity is the heritable condition that explains how environmental and genetic factors interact in ADD. Put simply, ADD is caused by the impact of the environment on particularly sensitive infants. At this point, we can start connecting the dots.
ADD rates are higher than ever – and they’re still rising, especially in developed nations like the United States. To cite just one eye-catching figure, there’s been a 36 percent increase in the reported prevalence of ADD in recent decades. What explains this trend?
It’s not genetics. Genes in a population don’t mutate over decades – such changes take hundreds, thousands, or millions of years. Yes, physicians are more likely to diagnose the disorder today than they were in the past. Similarly, there’s less stigma around mental health disorders, which means more people are seeking diagnoses. But those factors alone can’t explain such a steep increase. So what’s left? Simple: life circumstance.
When we try to explain today’s epidemic of obesity in countries like the United States, we look at changing lifestyles, not genes. So let’s apply that lens to ADD. Recall what we said about infants and their environment. Attunement, the emotional bond between child and caregiver, plays a critical role in cognitive development. The question is, has something changed in the parenting environment in recent decades which might be getting in the way of attunement?
Yes! Numerous studies show that Americans are more socially isolated than ever before. People have fewer friends and live further away from their families. They work more, too – in two senses. First off, they work longer hours. In 1935, the average worker had 40 hours of free time a week; by 1990, free time was down to just 17 hours. It’s also more common for both parents to work full-time jobs. Private childcare is expensive, and subsidized childcare is badly underfunded. Parental leave is patchy and, generally, short. As a result, caregivers have less time for their children. They are also more likely to be stressed. Wages are stagnating, and fraying community and family ties mean they have access to smaller and smaller support networks.
Why is the rate of ADD so high? For the same reason that rates of heart disease, diabetes, and obesity are so high. Today’s North American way of life fails to serve basic human needs. Miswired ADD circuits of the prefrontal cortex are as much evidence of this fact as the cholesterol-clogged arteries causing coronary disease.
Add these factors up and you get a simple equation. Caregivers are more likely to be stressed, depressed, and distracted from parenting than at any point in recent history. Despite their best intentions, these stresses interfere with their ability to sustain attuned relationships with their children. The resulting style of stressed parenting undermines children’s sense of emotional security, which interferes with the development of the brain structures that regulate focus, attention, and impulse control. The kids most dramatically affected by these trends are hypersensitive children – the children who are most likely to develop ADD.
Final Summary
The real issue when it comes to treating ADD isn’t about regulating behavior with psychostimulants – it’s about promoting the development of the child. And to address that issue, we can’t just look at the child individually. We also need to consider the familial and social context in which parenting and childhood development take place.
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