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64 pages 2 hours read

Gabor Maté

Scattered Minds: The Origins and Healing of Attention Deficit Disorder

Gabor MatéNonfiction | Book | Adult | Published in 1999

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Part 2Chapter Summaries & Analyses

Part 2: “How the Brain Develops and How the Circuits and Chemistry of ADD Arise”

Part 2, Chapter 6 Summary: “Different Worlds: Heredity and the Environments of Childhood”

Maté suggests that the prevalence of genetic fundamentalism, or the belief that all illnesses can be explained by heredity, has undermined a complete understanding of ADD. He calls the approach socially conservative and incurious about how society might affect a person’s psychological or emotional development. Maté doesn’t deny the genetic component of ADD, but he says that genes only represent potentials and that the expression of genes is mostly the product of environment. Maté cites a study into Huntington’s disease, a fatal disease with a strong genetic connection. Even so, some with the gene never develop the disorder. Another study, which studied diabetes rates in the Cree population of Ontario, provides evidence that the destruction of the traditional Cree lifestyle better correlates with predisposition to the disease than genes do. Maté concludes that the existence of an ADD gene, if proven, would not produce ADD on its own. Problems of the mind-body, Maté says, are more frequent when there is dysfunction in the family and in the parents’ lives.

Maté believes that twin studies are often interpreted incorrectly. According to research, twins adopted into separate homes have similar chances of experiencing ADD. This concordance is taken to prove ADD’s heritability, but Maté says that it is the disruptive conditions of adoption that are likely responsible. He is convinced that psychological tension and social stresses in the parents’ lives during their children’s infancy are the most important factors in the emergence of ADD.

Maté says that long-term healing is possible based on changing environments. Maté cites the example of Gary Gilmore, a murderer who was executed in the late 1970s—a sentence he didn’t appeal. Gilmore’s life was filled with trauma and violence, though his brother, Mikal, didn’t experience the same traumas because he was born when his parents were experiencing relative stability. No two siblings have the same parental experience, Maté says. The parents’ expectations fall most notably on firstborn children, Maté suggests. He cites studies that show that birth order has a dramatic impact on shaping personality. It is the psychological tension of the parents, as well as the part of themselves they see in the child, that best explains the emergence of ADD.

Part 2, Chapter 7 Summary: “Emotional Allergies: ADD and Sensitivity”

Maté poses a hypothetical parenting situation to illustrate the way sensitivity in a child may trigger sensitivity in the parent, which can lead to cycles of reactivity in the relationship. Allergies, Maté says, represent a kind of hyperreactivity to physical stimuli. ADD represents hypersensitivity to emotional stimuli. This, to Maté, is the heritable aspect of ADD. Having ADD, he says, is like having an exposed nerve. Individuals with ADD may be told they are overreacting or difficult and often display hyperreactivity. Maté claims that this difference in emotional reactivity is physiological: It is not a choice but a reflection of their surroundings, meaning that their reactions can be a good litmus test for their emotional environments. Maté points out that around one third of the North American population experiences conditions such as ADD, depression, or alcoholism. Maté says that the prevalence of these conditions represents an evolutionary predisposition for sensitivity. He sees this as an advantage since sensitive people may be better at expressing the urges and needs of humanity.

Part 2, Chapter 8 Summary: “A Surrealistic Choreography”

Biological heredity cannot account for the infinite, subjective potential of the brain’s microcircuitry, Maté says. That three quarters of brain development occurs outside the womb is evidence of human susceptibility to environment. Maté describes the development of the frontal lobes, which he says are responsible for problem-solving and social and linguistic skills. Maté describes a process called neural Darwinism in which nerve cells compete to survive. Unused neural pathways die off, and the brain loses the capacity to produce certain underutilized neurochemicals; for instance, the capacity for eyesight in infants will atrophy if unused. ADD, he says, is another such example of neurophysiology responding to environment. He lists three necessary conditions for healthy brain development: nutrition, physical security, and an unbroken relationship with a safe, maternal presence. Maté calls this third condition the “attachment relationship.” It is, he says, the one most likely to be disrupted in Western societies. Maté believes that when the neurophysiological development of self-regulatory circuits in the brain is disrupted, ADD may be the result.

Part 2, Chapter 9 Summary: “Attunement and Attachment”

Maté argues that ADD originates in the stresses that affect the primary caretaker’s emotional interactions with the infant. Attunement and attachment inform the emotional language between parent and child. Maté believes that these largely nonverbal messages are important aspects for infant development. Odor alone is responsible for developing millions of neural pathways in the infant’s brain in the first moments after birth. After just a few weeks, the infant already prefers the mother’s face to the face of a stranger or another parent, and the eyes of the infant follow the mother’s eyes closely by around 17 weeks.

Maté cites a study from the University of Washington that found that electroencephalograms can register the effect eye contact has on the brain. In the brain’s left hemisphere, low electrical activity is associated with depression, whereas positive emotions are associated with increased electrical activity in this region. To test this, the study placed mothers and infants in separate rooms and had them interact via closed-circuit television. At one point, the mothers were replaced by recordings of themselves. The infants began to react negatively to the recordings. Another study done by a researcher at the University of Cambridge found that diminished infant attention spans were associated with maternal depression.

Maté concludes that the infants in these studies responded poorly because they needed to feel their mother was participating in their emotional states—a state Maté calls “attunement” and views as necessary for the development of emotional self-regulation. Maté quotes attachment theorist John Bowlby, who says that mothers must regulate their emotional responses to integrate with their children. As an infant develops, Maté says, they will begin breaking attunement naturally to cool down their nervous system. This is an aspect of self-regulation. An anxious mother might react to this by trying to draw the infant’s attention back to herself, which may undermine the infant’s ability to learn self-regulation. The lack of healthy and dependable attunement is, to Maté, the origin of ADD. He cites addiction and fanatical religiosity as other potential reactions.

Part 2, Chapter 10 Summary: “The Footprints of Infancy”

The orbitofrontal cortex (OFC) is the portion of the brain behind the right eye; it tends to dominate the left hemisphere. ADD is not the product of only one brain center, though of all the parts of the brain, Maté says the OFC is the most affected by a lack of attunement. This is also the portion of the brain that controls self-regulation, social intelligence, and short-term memory. Maté speculates that this visual-spatial component may explain the experience of bumping into things common among people with ADD. The OFC controls attention by constantly processing emotional information: It is “deeply concerned with the assessment of relationships between the self and others” (79). The capacity for impulse control is also a product of the OFC, which delays reactions so that more sophisticated intellectual and emotional responses can emerge. The infant’s earliest emotional interactions in the world are imprinted on the OFC, Maté says, as the unconscious place from which all future emotional reactions will form. People with brain damage to the OFC often have symptoms that look similar to ADD. The ADD brain is not damaged, Maté says, but it has been impaired in its development in a way that simulates this type of brain injury.

The relationship between frontal lobe neurochemistry and psychological states is ignored by much of the medical community, Maté says, leading to the overprescription of medication aimed solely at altering brain chemistry. The common medical analysis is that depression represents a lack of serotonin and that ADD represents a lack of dopamine, both of which correspond to reward states. This is why Prozac and Ritalin, which provide these chemicals, are thought to help patients with depression and ADD, respectively. Maté quotes neurologist Antonio Damasio, who warns against ascribing causality to the presence of neurochemicals. To illustrate this, Maté cites studies into the effects of serotonin on the dominance of male monkeys. The research showed an increase in serotonin only after establishing dominance, suggesting that serotonin represented a maintenance factor in dominance rather than a causal factor. A 1998 study into rat behavior found that “early interactions with the mother shaped the adult rat’s capacity to respond to stress” (83). Another study showed the negative effects of isolation on this development. These studies suggest that neurophysiological serotonin and dopamine receptors are produced in response to environmental stimulation. Imbalanced brain chemistry, Maté says, is both the cause and effect of emotional experiences.

Part 2 Analysis

Maté believes that it is erroneous to describe the vast complexities of the ADD experience with something like biology, which he depicts as comparably straightforward. For example, genetic explanations fail to account for all the people who possess the associated gene who do not exhibit the disorder. Maté is more interested in establishing what developmental factors are responsible for the activation of genes. Predisposition, to Mate, is helpful only insofar as it helps a patient to contextualize their experience within a social and intergenerational framework. To that end, Maté reevaluates the use of twin studies in understanding psychological outcomes, recasting studies typically understood to demonstrate the influence of genetics (because identical twins possess virtually the same DNA) as instead demonstrating the influence of environment.

Maté suggests that this environmental view of ADD is inherently optimistic because it implies sociological solutions. “Historical or social circumstances,” Maté writes, “may have enormous consequences on the parent’s emotional states and therefore on the personalities of their children” (54). Locating societal problems in the individual is, to Maté, an inherently conservative outlook on psychological and developmental disorders: He believes that the medical community would prefer to treat the symptoms of these disorders individually because it enforces personal responsibility and allows pharmaceutical companies to prescribe medication. Though Maté values medication, he calls it a stopgap measure, arguing that no real healing can occur until the social pressures on the family (and thus on early childhood development) are eased.

More specifically, Maté believes that it is parents’ unprocessed trauma projected onto children that causes ADD to develop. Maté does reserve a role for heritability, arguing that sensitivity, especially emotional sensitivity, predisposes one to develop ADD as well as associated conditions like addiction. He uses the metaphor of an allergy to explain the way sensitive infants may be susceptible to emotional pain. Even here, however, Maté expresses Skepticism of the Illness Model in ADD Awareness and Treatment by suggesting that sensitivity is not inherently pathological. Rather, Maté believes that this evolutionary predisposition for sensitivity is an important aspect in the development of creativity and that it represents an intrinsic tool for the survival of the human species.

The attunement relationship between a mother and an infant is the core of Maté’s model of ADD, and it is in this section that Maté fully introduces The Centrality of the Attunement Relationship to the Development and Healing of ADD. The fully realized human cannot develop a core sense of self, he says, without proper nutrition, physical safety, and “an unbroken relationship with a safe, ever-present maternal organism” (66). Maté doesn’t think this primary caregiver has to be the child’s biological mother—or, indeed, a woman at all—but that caregiver does need to mirror the infant’s behavior and offer the infant a sense of “unconditional positive regard.”  Drawing on attachment theory as a model, as well as Erik Erikson’s stages of development, Maté argues that brain development hinges on a secure relationship with one’s parents.

According to this theory, ADD is the result of the underdevelopment of circuits in particular areas of the brain: “It is not that a disorder develops, but that certain important brain circuits do not develop” (80). The impact of this is complex, but Maté believes that recognizing it is the only path to healing. By specifically identifying the different developmental stages of the brain and by locating within each stage of infant development a corresponding ADD symptom, Maté makes it possible for people with ADD to make sense of their emotional experiences and provides an organized path toward healing.

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