The Deepest Well: Healing the Long-Term Effects of Childhood Trauma and Adversity—A Transformative Guide to Understanding Childhood Trauma and Health

by Nadine Burke Harris

Twenty years of medical research has shown that childhood adversity literally gets under our skin, changing people in ways that can endure in their bodies for decades. It can tip a child’s developmental trajectory and affect physiology. It can trigger chronic inflammation and hormonal changes that can last a lifetime. It can alter the way DNA is read and how cells replicate, and it can dramatically increase the risk for heart disease, stroke, cancer, diabetes—even Alzheimer’s.

During one of my trips down the research rabbit hole, I found some great work by Jacqueline Bruce, Phil Fisher, and colleagues. In a 2009 study, they set out to determine if the adverse experiences of preschool-age foster children had an effect on the functioning of the stress-response system, specifically the HPA axis. To do this, they analyzed the cortisol levels of 117 foster kids and 60 low-income kids who were not maltreated. What they found reinforced what I suspected about my own patients: the foster kids showed dysregulated cortisol levels in comparison to the kids who had not experienced the same adverse experiences.

The main issue is that when the stress response is activated too frequently or if the stressor is too intense, the body can lose the ability to shut down the HPA and SAM axes. The term for this is disruption of feedback inhibition, which is a science-y way of saying that the body’s stress thermostat is broken. Instead of shutting off the supply of “heat” when a certain point is reached, it just keeps on blasting cortisol through your system. This is exactly what Fisher and Bruce were seeing in the foster kids.

Apart from these revelations, the profound discovery was that our patients with four or more ACEs were twice as likely to be overweight or obese and 32.6 times as likely to have been diagnosed with learning and behavioral problems.

In Europe, hyperthyroidism is often called Basedow’s disease, after Karl Adolph van Basedow, the German physician who described the condition contemporaneously with Dr. Robert Graves. In my research on toxic stress, I had come across some data describing the high number of cases of hyperthyroidism among refugees from Nazi prison camps. In fact, the term kriegs-Basedow (kriegs means “war,” so kriegs-Basedow is “hyperthyroidism of war”) was coined following the observation of an increased incidence of hyperthyroidism during major wars. Trinity

In the previous chapter, I mentioned that a graph of the response of the prefrontal cortex to adrenaline and noradrenaline looks like an inverted U. Well, for kids with impaired impulse control and inattentiveness due to toxic stress, PFC function is likely to be on the downslope of the inverted U (kind of like if you drink way too much coffee, you can’t focus to save your life). In those cases, our clinical team tends not to use stimulants like methylphenidate (Ritalin) or drugs derived from amphetamines. Instead, we often use guanfacine, a nonstimulant that was originally developed to treat high blood pressure but has also been used to treat ADHD. Guanfacine targets specific circuits in the prefrontal cortex where adrenaline and noradrenaline exert their action, improving impulsiveness and concentration, even in situations of high stress.

MRI studies of severely maltreated kids from Romanian orphanages shows dramatic enlargement of their amygdalae. The other thing that happens when the amygdala is chronically or repeatedly activated is that it starts messing up its predictions about what’s scary and what’s not. The amygdala begins sending false alarms to the other parts of your brain about things that shouldn’t actually be scary, just like the little boy who cried wolf.

For kids with toxic stress, the activity of the prefrontal cortex is inhibited in two ways. First, the overactive amygdala sends messages to the PFC telling it to decrease its functioning because something scary is happening; you don’t want reason getting in the way of survival. The second is that the locus coeruleus is flooding the brain with noradrenaline, compromising the ability to override instincts and impulses. The PFC is the part of the kid’s brain that puts the brakes on impulses and helps him or her make smarter decisions. Telling a kid to sit still, concentrate, and ignore stimuli that are flooding his brain with the need to act is a lot to ask. This down-regulation of the PFC can have different consequences for different people. For some, it results in an inability to concentrate and solve problems, but in others it manifests as impulsive behavior and aggression.

The hippocampi are two cute little seahorse-shaped parts of the brain responsible for creating and maintaining memory. When the amygdala gets activated during a major stress event, it sends signals to the hippocampus that disrupt its ability to knit together neurons, essentially making it more difficult for the brain to create both short-term and long-term memories. On brain scans of patients with Alzheimer’s disease, the hippocampi are badly damaged. Knowing that, it’s pretty obvious why this part of the brain is so critical to learning, and it’s easy to see how kids with quick-trigger amygdalae are behind the eight ball when it comes to everything from memorizing multiplication tables to spatial memory.

When your body’s stress-response system is overloaded again and again, it messes with the sensitivity of your dopamine receptors. You need more and more of the good stuff to feel the same amount of pleasure. The biological changes in the VTA that lead people to crave dopamine stimulators like high-sugar, high-fat foods also lead to an increase in risky behavior. The ACE Study shows that there is a dose-response relationship between ACE exposure and engaging in many activities and substances that activate the VTA. A person with four or more ACEs is two and a half times as likely to smoke, five and a half times as likely to be dependent on alcohol, and ten times as likely to use intravenous drugs as a person with zero ACEs.