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.

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.

Toxic stress response can occur when a child experiences strong, frequent, and/or prolonged adversity—such as physical or emotional abuse, neglect, caregiver substance abuse or mental illness, exposure to violence, and/or the accumulated burdens of family economic hardship—without adequate adult support. This kind of prolonged activation of the stress-response systems can disrupt the development of brain architecture and other organ systems, and increase the risk for stress-related disease and cognitive impairment, well into the adult years.

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. So for anyone looking to prevent young folks from developing dependencies on bad-for-you dopamine stimulators like cigarettes and alcohol, understanding that exposure to early adversity affects the way dopamine functions in the brain is an absolute must.

The “lick your pups” study is a great example of this type of epigenetic regulation. Meaney and his team found that high-licker moms were releasing high levels of serotonin in their offspring. You may have heard that serotonin is the body’s natural antidepressant. It boosts mood and acts as the equivalent of rat-pup Prozac. This serotonin didn’t just make the pups feel better, it also activated a chemical process that changed the transcription of the part of the DNA that regulates the stress response. Meaney and colleagues eventually demonstrated that all that licking and grooming ultimately changed the epigenetic markers on the rat pups’ DNA, leading to lifelong changes in the stress response. This kind of epigenetic change is like a communication shortcut for nature. When rat moms don’t lick their pups, they are essentially telling them that there is something to be wary about in the environment, so they should be on high alert. Instead of waiting around for the generations-long process of genetic adaptation to change the offspring’s DNA, this environmental information gets passed on to the rat pup quickly through a change in the epigenome. To look more closely at this process, the Meaney research team did something brilliant; taking a cue from a Lifetime TV movie, they switched some of the rat pups at birth. They placed pups of high-licker moms with moms who were low lickers, and vice versa. The study found that the pups’ DNA methylation took on the pattern of their fos...

Further work by researchers Aoife O’Donovan and Thomas Neylan compared the telomeres of people with PTSD with the telomeres of people in good mental health. What they found was that overall, those with PTSD had shorter telomeres than those in the control group. However, what was really interesting was that the people with PTSD who did not have early childhood adversity didn’t tend to have shorter telomeres. The good news is that even if you have shortened telomeres, maintaining healthy telomeres can protect you from further shortening. How do you keep your telomeres healthy? One important way is by boosting levels of telomerase, which is an enzyme that can actually lengthen the telomere. Once again, the science is new, but it suggests that even if you start out with shorter-than-normal telomeres, you can still slow decline by increasing your telomerase with things like meditation and exercise.

Dr. Lieberman debunked the long-held myth that young children and babies don’t need treatment for trauma because they somehow don’t understand or remember the chaotic experiences they faced. Her work is built on research that shows that early adversity often has an outsize effect on infants and young children, just like it did on Dr. Hayes’s tadpoles. After years as a clinician, Dr. Lieberman came to understand that children’s need to create a story or narrative out of confusing events is actually very normal. Children are compelled to give meaning to what is happening to them. When there is no clear explanation, they make one up; the intersection of trauma and the developmentally appropriate egocentrism of childhood often leads a little kid to think, I made it happen.

CPP takes into consideration all the other pressures and drama that both parent and child have to deal with—other family members, the community, work (or lack thereof)—everything that affects the parent-child bond. This allows patients to make connections between the traumas of the past and the stressors of the present, so they can better recognize their triggers and manage their symptoms. Traditionally, if a mom is depressed, she finds her own therapist and they work one on one. CPP’s approach is based on the understanding that the quality of the relationship and the health of the attachment between the parent and child are absolutely fundamental to health and well-being.

Sleep helps properly regulate both the HPA and the SAM axes. During sleep, levels of cortisol, adrenaline, and noradrenaline drop. As a result, lack of sleep is associated with increased levels of stress hormones and increased stress reactivity. As you know from Chapters 5 and 6, these stress hormones kick off the party, triggering brain, hormone, immune, and epigenetic responses to stress. The downstream effects are impaired cognitive function, memory, and mood regulation. Sleep deprivation doesn’t just make you groggy and cranky; it also makes you sick. Lack of sleep is associated with increased inflammation and reduced effectiveness of the immune system.

Slowly but surely, we were building our toolkit of clinical interventions to combat the effects of toxic stress. Sleep, mental health, healthy relationships, exercise, nutrition, and mindfulness—we saw in our patients that these six things were critical for healing. As important, the literature provided evidence of why these things were effective. Fundamentally, they all targeted the underlying biological mechanism—a dysregulated stress-response system and the neurologic, endocrine, and immune disruptions that ensued.

Why were people so resistant to the science of adversity and to giving a basic fact of our biology a name and a number? Because when you bring it down to the level of cells, the level of biological mechanisms, then it is about all of us. We are all equally susceptible and equally in need of help when adversity strikes. And that is what a lot of folks don’t want to hear. Some want to stand back and pretend that this is just a poor-person problem. Others take fierce ownership of the problem and say, “This is killing my community,” but what they also mean is It’s killing my people more than yours. In rural white communities, the story is about loss of living-wage work and the fallout from rampant drug use. In immigrant communities, it is about discrimination and the fear of forever being separated from loved ones at a moment’s notice. In African American communities, it’s about the legacy of centuries of inhuman treatment that persist to this day—it’s about boys being at risk when they are playing on a bench or walking home from the store wearing a hoodie. In Native American communities, it is about the obliteration of land and culture and the legacy of dislocation. But everyone is really saying the same thing: I am suffering. It is easy to get stuck on your own suffering because, naturally, it is what affects you most, but that’s exactly the mentality that is killing black people, white people, and all people. It perpetuates the problem by framing it in terms of us versus th...

We were giving Diego state-of-the-art care. The problem is that the state of the art sucks.

My experience dealing with both sides of the ACEs coin is in part what drives my work. I know that the long-term impacts of childhood adversity are not all suffering. In some people, adversity can foster perseverance, deepen empathy, strengthen the resolve to protect, and spark mini-superpowers, but in all people, it gets under our skin and into our DNA, and it becomes an important part of who we are. I don’t think people who grew up with ACEs have to “overcome” their childhoods. I don’t think forgetting about adversity or blaming it is useful. The first step is taking its measure and looking clearly at the impact and risk as neither a tragedy nor a fairy tale but a meaningful reality in between. Once you understand how your body and brain are primed to react in certain situations, you can start to be proactive about how you approach things. You can identify triggers and know how to support yourself and those you love.