The Deepest Well: Healing the Long-Term Effects of Childhood Adversity

Burke Harris dives deeply into the effect of the toxic stress response on multiple systems in the body. She explores how her growing understanding of its effects began to shape her approach to diagnosing and treating her patients in Bayview.

She noted early on that her patients tended to come into her clinic with significant learning challenges. Early and extreme adversity has a big effect on the brain, so she wasn’t surprised by the high rates of educational challenges.

Toxic stress measurably affects the function of key aspects of the neurological system. The amygdala, which controls fear responses, is larger in children with higher occurrences of ACEs. Children overreact to perceived danger as a result. The locus coeruleus is a part of the brain that helps it choose when to engage in aggressive behavior and manage impulses. Adversity causes too much noradrenaline (a neurotransmitter) to circulate in the brains of traumatized children, so they may be more aggressive and impulsive.

The prefrontal cortex, which Burke Harris compares to a conductor of the symphony, is responsible for reason, reflection, and executive functioning (the prioritizing and planning necessary for good decision-making). Under the influence of toxic stress, the prefrontal cortex is smaller, making it harder for children to exercise impulse control.

The hippocampus is another key part of the neurological system. It’s the memory center of the brain, and toxic stress dampens its ability to make long- and short-term memories—a real problem since memory plays a key role in learning.

The ventral tegmental area controls “rewards, motivations, and addictions” (69). When toxic stress interferes with the proper functioning of this part of the neurological system, children (and the adults they become) tend to have problems with behaviors influenced by impulse control and dopamine (the pleasure hormone). They thus may have higher rates of addiction, smoking, consumption of high-fat and high-sugar foods, and the negative outcomes associated with lack of impulse control.

Furthermore, the enduring problems associated with the toxic stress response disrupt the proper functioning of hormones, the “body’s chemical messengers” (70) that regulate biological functions. Visible effects like Diego’s lack of growth or obesity in Burke Harris’s patients reflect the influence of hormonal disruption caused by toxic stress.

The effect of toxic stress shows up in the immune system as well. Under a constant barrage of cortisol and stress, the body’s immune system uses its weapons—cytokines (for example, white blood cells that activate cells to attack and clean up unhealthy cells and invaders) and inflammation to be ready for assaults to the immune system. The body isn’t meant to be on high immune alert permanently, however, so autoimmune diseases like asthma and allergies are rife among children with a history of many ACEs. These overactive immune responses persist even after such children grow up and escape the immediate adversities in their lives.

In her practice, Burke Harris noted just what she would expect to find in children with much adversity in their lives. They had higher rates of obesity, learning differences, and autoimmune illnesses. Under the influence of her research and field observations, Burke Harris and her staff made questions about ACEs a standard part of intake and crafted her diagnoses and treatments to address what she was learning about the effect of toxic stress.

For example, Trinity was a young girl with behavioral and legal problems that seemed to arise each time her mostly absent mother with a heroin addiction involved her in shoplifting. Trinity’s aunt, her caretaker, came to the clinic seeking an official diagnosis of attention deficit hyperactivity disorder (ADHD), but Burke Harris took a different approach. She examined Trinity physically and discovered that Trinity had Graves’ disease, an autoimmune disorder resulting from too much thyroid hormone in the body. Thyroid treatments to address this autoimmune disorder and talk therapy to reduce the toxic stress that was likely playing a role in the autoimmune disorder—not stimulants like Ritalin—were the right approach for Trinity. Using what she’d learned about toxic stress was already changing Burke Harris’s approach to treating her patients.

As Burke Harris continued her work in Bayview, she generated questions about the influence of the ACEs on parents and caretakers of her young patients. Her reading of Felitti et al had already revealed that a protective caretaker could blunt the effect of adversity and short-circuit the transformation of the stress response from positive/tolerable to toxic. This knowledge eased Burke Harris when she had to call Child Protective Services (CPS) in any case where it became clear that her patients’ parents or caretakers couldn’t provide care that would allow a child to thrive physically and behaviorally. In one case, she called CPS regarding a young mother, Charlene, whose prematurely born daughter, Nia, failed to thrive under her mother’s care in part because Charlene seemed emotionally disconnected from Nia.

Ever the researcher, Burke Harris uncovered two significant studies that clarified the mechanism by which caretakers could ease the influence of the toxic stress response in children. The first study was on the influence of the behavior of rat mothers on rat pups. Rat pups whose mothers lick them often—nurturing behavior that increases the serotonin of the pups and reduces the stress response that the pups experience after researchers handle them—have better long-term health outcomes than pups whose mothers lick them only a little. Researchers also noticed that one can change the stress response of pups by switching them from high-licking mothers to low-licking mothers and vice versa. These changes in the stress response persist throughout the rat’s life and beyond: In subsequent generations, the high-licking and low-licking mothers transmit their respective behaviors to their offspring.

Even more exciting for Burke Harris about this research was that it might reveal the mechanism for what she calls “multigenerational ACEs” (83). Burke Harris explains that who we are in terms of our bodies results from our DNA (genome) and from epigenomic regulation—the interaction between stressors in our environment and the epigenome, the system that controls whether a gene is expressed. People potentially inherit from their parents both genes and the epigenetic shifts that control the expression of genes. Epigenetic shifts act more quickly than long-term genetic adaptation over generations; the importance of epigenetic regulation of gene expression is that parents who experience ACEs that lead to toxic stress responses may hand down a maladaptive stress response to the next generation through their genome and epigenome, not just through their parenting.

Additional research added another wrinkle to Burke Harris’s understanding of the relationship between genes and the environment. Telomeres, “noncoding sequences” (87) of DNA that help ensure exact copies of genes, are some of the first parts of the genome to respond to stressors. They shorten in response to stressors (including ACEs). Once damaged, they tell nearby cells to die or else stop functioning (leading to diseases). Shortened telomeres may also allow cells to reproduce without limits (i.e., cancer). Research shows that ACEs in childhood are associated with shorter telomeres in adulthood. The same relationship doesn’t apply to adults who experience adversity in adulthood but not in childhood.

Epigenetic regulation and telomeres do respond to intervention measures that reduce toxic stress if those measures happen early. Burke Harris concluded that a protocol to identify children most at risk for ACEs leading to toxic stress responses was necessary. Such a protocol would enable healthcare providers to get children the help they needed to escape multigenerational genetic effects and the health disparities that resulted from their own ACEs.

Her first effort to sound the alarm about this research was to present her findings to the Hospital Council of Northern and Central California, a group tasked with, among other things, addressing health disparities. Her presentation failed: The mostly white and male group (except for a woman clearing their dishes) showed little interest in acting. They understood what she was saying, but she didn’t come to them with clear-cut solutions and a protocol to implement. She felt some despair about their response and began to wonder if her desire to intervene in the effects of ACEs on her patients was naive and doomed.