PARENTS OF VERY YOUNG babies come into my clinic displaying all the different colors of the emotional rainbow—exhausted, elated, concerned, proud, terrified. So when Charlene brought her daughter, Nia, in to see me, Charlene’s complete lack of facial expression stood out. When I asked this young mother a question about her daughter, she would respond, but her face and eyes stayed flat. It was almost as if we were talking about what size shoe she wore or what time the number 22 bus would arrive. Otherwise, she could have been any early-twenty-something mom with an infant; she was snugly tucked into jeans and wore a cute blouse with her hair pulled back neatly. Five-month-old Nia, however, was not typical—when Charlene was pregnant with her, Nia had stopped growing and had to be delivered by emergency C-section eight weeks early; at birth, she had clocked in at a mere three pounds. After weeks in the hospital, Nia improved nicely and was released in good health, but in the weeks that followed at home, she had struggled to gain weight.
As I worked with my team and Charlene to figure out the cause, I became increasingly concerned. We spent hours walking Charlene through how to prepare food for her daughter, when to feed her, and how much to give her. We took Nia’s vitals and did blood work. We watched her weight and height measurements like mission control for the space shuttle launch. All the while, Charlene, too, was coming into clearer focus. Moving beyond her characteristic flatness, she would quickly become annoyed and overwhelmed when her daughter would cry or fuss. She’d tell her to shut up or ignore her completely. It looked to me like a clear case of postpartum depression, but no amount of urging could convince Charlene to get help.
Eventually, Nia’s health became critical and we were out of options. She was suffering from failure to thrive, a medical term that describes babies who don’t gain enough weight and eventually can’t meet their developmental milestones. Every second in the first years of life over one million new neural connections are formed, so if an infant isn’t getting enough fats and proteins needed to make healthy brain connections, that can have significant impacts. I recommended that Nia be hospitalized, hoping that under constant care, she would gain the weight she so desperately needed. Nia spent four days in the hospital and did exactly that, but soon after she was released, the gains she made were erased. We redoubled our efforts, bringing in our social worker and trying hard to engage Charlene in treatment, but eventually we had to send Nia for yet another hospital stay. This time, when I talked to the inpatient team at the hospital, we agreed that it was time to start talking about Child Protective Services (CPS). They were seeing the same problems with Charlene and Nia’s dynamic that we were. Charlene was still suffering from depression, and she was still refusing to get help. After Nia was released the second time, she again failed to grow and thrive at home. With a heavy heart, knowing Charlene would be thrown into a tailspin, I had to do something no pediatrician ever wants to do—file a CPS report.
I didn’t know for sure that Charlene was being overtly neglectful, not feeding Nia, or hurting her, but I did know that Nia was way below the third percentile for weight even when we took into account her prematurity. She was in the danger zone and it was clear by then that the dynamic between daughter and mom was affecting Nia’s growth. In cases like this, it can be hard to parse things out. We know that babies who are born premature are at greater risk of neglect simply because they have greater needs—more irregular sleep patterns, more frequent feedings—and that those needs can be enough to overstress an exhausted new parent. But if an infant doesn’t have a caregiver’s reciprocal eye contact, stimulating facial expressions, snuggles, and kisses, hormonal and neurologic damage can occur, and that can prevent a child from growing and developing normally. When a baby is not being cared for, she doesn’t grow well, even if she has enough nutrition. Was Nia’s problem that she wasn’t getting enough food? Or was it that Charlene was so depressed she wasn’t stimulating Nia? The truth was that it could have been both.
Here’s where I put my toxic stress lens on the situation. At the tender age of five months, with a depressed mom and a dad who wasn’t involved, Nia already had two ACEs. I had some strong suspicions that Charlene had an ACE score as well. Despite the initial sadness I felt at having to file the report and put Charlene under the strict eye of CPS, a major question I’d had before came bubbling to the surface once again: How is it that ACEs are handed down so reliably from generation to generation? For many families, it seemed that toxic stress was more consistently transmitted from parent to child than any genetic disease I had seen.
Take, for example, Cora, a longtime Bayview resident who was the primary caregiver for ten-year-old Tiny, her great-grandson. At sixty-eight, Cora had not intended to raise another child, but when the child welfare workers called to say that Tiny’s mom was incarcerated and they needed to find a home for the boy, Cora felt torn. Her son, Tiny’s grandfather, wasn’t capable of caring for a child. Both he and Tiny’s grandmother had struggled with addictions to alcohol and other substances, and she had passed away from kidney failure in her late forties. Now it looked like Tiny’s mother would be in prison for a long time. Cora was exhausted. Still, she couldn’t let the boy go into the system.
Cora brought Tiny in to see me for his regular checkup. Her greatest concern was his behavior. She received calls from the school on a daily basis. Most recently, he had overturned his desk in class, and when the teacher pulled him aside to reprimand him, Tiny had kicked her, earning him a suspension. During the exam, I got a chance to see what Cora was talking about. Most kids are on their best behavior in the doctor’s office, so observing Tiny was revealing. He would frequently interrupt, aggressively rip up the exam table’s paper to get our attention, and then leap off the table, open drawers, and pull out whatever was inside. At one point, he scooted down on the floor and managed to unplug my computer before I could redirect him. No doubt, staying ahead of Tiny was a workout.
Cora and Tiny’s visit was in the early days of the Bayview clinic, back before we were doing regular ACE screening, but I could tell he would need a lot of resources. I excused myself for a moment to knock on Dr. Clarke’s door for a brief consultation. When I returned to the room, I opened the door the same way I always did, with a brief “Knock, knock” before I gently swung the door open. The scene I walked in on stopped me in my tracks.
Tiny crouched in the corner, his hands shielding his face from the blows his great-grandmother was raining down on him. Shoulders, head, face, body—Cora was slapping and yelling, really going at him.
I almost couldn’t believe my eyes. Was she seriously beating the child in the doctor’s office?
“Stop!” I said forcefully. I crossed the room in two strides and physically inserted myself between them. “You’re not allowed to hit children in our clinic or anywhere else.”
I gave Tiny a good once-over to make sure that he wasn’t seriously injured. Then I calmly explained to Cora that because I was a mandated reporter, I would have to call CPS.
“Go on an’ call ’em,” Cora responded. “CPS don’t got to raise that baby, I do. He need to get some act-right in him. Otherwise, he goin’ to end up in the pen just like his mama.”
It was obvious to me that Cora believed that she was doing the right thing. After watching two generations lose their way, Cora was relying on the tools she had learned in her own upbringing to keep Tiny on the straight and narrow. The irony was that, despite Cora’s intentions, the beating was undoubtedly unleashing a neurochemical cascade that made Tiny more likely to end up like his mom and his grandparents. That day, I convinced Cora to sit with me as I made the call to CPS. She got to see that I wasn’t “ratting her out” but rather advocating for her, telling the agency that she needed additional tools to help her manage Tiny’s challenging behavior without using violence. Ultimately, she trusted me enough to agree to work with Dr. Clarke; the beatings stopped, and the family remained intact.
For a long time, that interaction with Cora stayed with me. I thought about her and Tiny and the generations in between. I was seeing all around me evidence of multigenerational ACEs. But it was rat mothers and rap pups in landmark studies by Dr. Michael Meaney and his colleagues at McGill University that helped me piece together how to understand and ultimately interrupt the biological legacy of toxic stress.
Meaney and his team looked at two groups of rat mothers and rat pups. They noticed that after the pups were handled by researchers, the moms would soothe their stressed-out pups by licking and grooming them. This is basically the human equivalent of hugs and kisses. What was fascinating was that not all moms did it to the same extent. Some moms exhibited high levels of licking and grooming behavior toward their pups. Other moms displayed low licking and grooming behavior, which meant they didn’t give as many sloppy kisses and embarrassing hugs when their pups were having a rough day.
Here’s the part that made me sit up straight in my chair: Researchers observed that the development of the pups’ response to stress was directly affected by whether the mom was a “high licker” or a “low licker.” They found that pups of high-licker moms had lower levels of stress hormones, including corticosterone, when they were handled by researchers or otherwise stressed out. This high-licker-leads-to-low-stress effect also showed a dose-response pattern: the more licking and grooming the rat pups got, the lower their levels of stress hormones. In addition, the pups of high-licker moms had a more sensitive and effective “stress thermostat.” By contrast, pups of low lickers not only had higher spikes of corticosterone in response to a stressor (in this case, being placed in restraints for twenty minutes), they also had a harder time shutting off their stress response than did the pups of high-licker moms. The licking and grooming behavior that occurred in the pups’ first ten days of life predicted changes to their stress response that lasted for the entire lifetime. Even more startling, the changes continued into the next generation, because female pups who had high-licker moms became high lickers themselves when they had their own kids.
I thought of Charlene and Nia as I read about Meaney’s work and I wondered how much “licking and grooming” Charlene herself had received as a child. She was certainly facing her fair share of stressors. I had witnessed in my residency how frightening it can be to have a premature infant, even for the most well-supported and resilient of parents. When she came through the door of my clinic, Charlene was the young, depressed mother of a premature infant, but she hadn’t always been that.
Growing up in Bayview, Charlene was full of promise. As a high-school soccer star, she seemed to have beaten the odds when her athletic prowess earned her a college scholarship. But a knee injury in her freshman year cut her dreams short. She dropped out the following year, and after a few years at home, she became pregnant. Now she was struggling to care for her baby girl. I worried for both Charlene and Nia. My medical training had taught me how to make the diagnosis of failure to thrive. What I hadn’t learned was how to break the intergenerational cycle of toxic stress.
I consumed Meaney’s research, searching for that all-important mechanism at the source. What the researchers were hoping to discover was how this early behavior could go on to affect the rats’ stress response and behavior for the rest of their lives. In other words, these scientists were looking for the root of the change. Just like me.
What they found was that the rat moms were, in fact, handing down a message to their pups that changed the way the pups’ stress responses were wired, but the mechanism, the how of the changes, turned out to be not genetic, but epigenetic.
Many people still think of genes and the environment as very separate things: you’re born with a certain genetic code that determines your biology and health and you have experiences that shape more malleable things like character and values. Keeping genes and environment in separate corners like this has sparked years of debate about which is more important, nature or nurture. People have been arguing over this for a long time, but as science gets more and more advanced, there is less and less to argue about. Scientists can now say pretty definitively that there is no separating the two. In fact, we now know that both environment and genetic code shape both biology and behavior. Considering how closely genes and environment work together, it’s no surprise that the debate raged on for hundreds of years with no winner in sight. Luckily, with the advances in science, we are finally able to see that there is a vital synchronicity that determines what we look like, how our bodies work, and ultimately who we are.
Most people know that DNA is the genetic code, the basic blueprint for your biology. To take that understanding a step further, your body uses this code as a template to produce the proteins that make up new cells and ensure that all the things inside those cells function. Every cell has your entire genetic code in it as well as the machinery to read the code and decide which parts of the sequence to translate into proteins.
Environment and experience play a huge role in determining which parts of your genetic code are read and transcribed in each new cell your body creates. How does your experience or environment do that? Well, it turns out that the body doesn’t actually “read” every “word” of its DNA. What scientists have discovered is that baked into the cells are both the genome (your entire genetic code) and the epigenome, another layer of chemical markers that sit on top of your DNA and determine which genes get read and transcribed into proteins and which ones don’t. The term epigenetic actually means “above the genome.” These epigenetic markers are handed down from parent to child along with the DNA.
One way to think about it is this: The genome is like the musical notes in sheet music and the epigenetic markers are like the notations that tell you how loudly, quietly, quickly, or slowly to play the notes. There might be a notation to skip an entire section of music altogether. These epigenetic notations are subject to experience, to being rewritten by your environment.
Activation of the stress response is one big way the environment can change epigenetic notations. As your body tries to adapt to the stress of your experiences, it turns certain genes on or off, particularly genes that regulate how you’ll respond to stressful events in the future. That process of the epigenome working with the genome to respond to your environment is called epigenetic regulation and it’s critical to our understanding of why toxic stress is so damaging to our lifelong health. When a four-year-old breaks a bone, that trauma is not encoded in his epigenome; it doesn’t affect him in the long term. But when a four-year-old experiences chronic stress and adversity, some genes that regulate how the brain, immune system, and hormonal systems respond to stress get turned on and others get turned off, and unless there is some intervention, they’ll stay that way, changing the way the child’s body works and, in some cases, leading to disease and early death.
There are a handful of processes that are responsible for epigenetic regulation, but the two that we know the most about when it comes to the genetics of stress are DNA methylation and histone modification. In DNA methylation, a biochemical marker called a methyl group is attached to the beginning of a DNA sequence. That marker prevents the gene from being turned on; it acts like a Do Not Disturb sign hanging on a hotel doorknob. It tells the DNA housekeeping team not to come in and translate that genetic sequence into proteins, essentially rendering that part of the genetic code silent.
Histones are like a chastity belt for the DNA. They are proteins that keep the genetic material locked up, preventing the DNA transcription machinery from getting to it. When certain biochemical markers are attached to the histones, the histones are then modified—they change shape and become more open, allowing the DNA to be read and transcribed. Which brings us back to the rat moms and their pups. 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 foster moms’, not their genetic moms’. So did their behavior—if a rat pup born to a high-licker mom was fostered by a low licker, she grew up to be an anxious adult rat with high levels of stress hormones who was a low licker herself when she had her own pups. Meany and his team found that the differences in licking and grooming that happened very early on (in this case, the first ten days of a rat pup’s life) made a huge difference.
To take it one step further, Meaney and his colleagues tested whether it was possible to reverse DNA methylation patterns after a rat had reached adulthood. Using trichostatin A, a solution capable of pulling methyl markers off DNA, they devised a way to chemically alter methylation patterns. When they injected the TSA solution into the brains of the adult offspring of both the high-licker and low-licker moms, it completely eliminated the changes in the adult rats’ stress response.
This study was a showstopper for me for a couple reasons. It showed the mechanism of these long-term changes was not simply genetic. The adverse experiences of my Bayview patients were factors that extended down to their DNA and likely changed them epigenetically.
Meaney’s work showed me not only how moms can negatively affect their pups by not licking them enough but also how they can help them by licking them more. The fact that environment is something we can modify means there is a lot of hope for human pups born to “low-licker” moms. These pups are not damaged goods; they are not defective. If they can get a safe, stable, and nurturing environment at an early age, the biology says that this sets them up to develop a healthy stress-response system in adulthood. As we’ve mentioned, the key to keeping a tolerable stress response from tipping over into the toxic stress zone is the presence of a buffering adult to adequately mitigate the impact of the stressor. In the case of the rat pups, it’s the mom’s licking and grooming. In the case of a human, it could be a dad hugging and listening. The buffer is hugely important, not just to attenuate the stress hormones but also to prevent the kind of epigenetic changes that lead to a dysregulated stress response and the major health issues that come with it.
But I still had some questions. We know that a rat pup whose mom was a low licker would likely have lifelong problems with the regulation of its stress response. And we also know that an overactive stress response can set off a cascade of changes to neurologic, endocrine, and immune function. But on the level of DNA, how does that chronic stress affect the likelihood of getting certain diseases, like cancer? After looking at how changes to the epigenome can be passed down from generation to generation, I wondered if higher risks for particular diseases became embedded as well. Was there some part of the DNA that got changed by stress and permanently turned on the genes for disease? Or was there something else going on? It wasn’t until I stumbled into the wild world of telomeres that I saw there was more than one way to reprogram DNA.
It’ll probably be no surprise that the only thing I love more than a badass scientist is a badass woman scientist. So you can imagine my excitement when I found out about a dynamic duo right in my own backyard. I was first introduced to the work of Dr. Elizabeth Blackburn and Dr. Elissa Epel of UCSF by a friend who has many lovely qualities but who also happens to be a little obsessed with premature aging. When it comes to aging, I tend to ignore the chatter and stick with clean livin’ and night cream, but when my friend dropped the words chromosomes and premature cell death into the conversation about the latest antiaging news item, my ears perked up. Turns out this was one legit scientific discovery in the quest to understand the aging process. Dr. Blackburn is one of three scientists who received the Nobel Prize for discovering how telomeres, the sequences on the ends of chromosomes, work to protect DNA from the kind of damage that can lead to premature aging and death. Blackburn teamed up with health psychologist Elissa Epel and the two took off on a research tear, exploring how exactly telomeres could be shortened or damaged and, more important, how to stop it.
Blackburn and Epel looked at how food, exercise, and even mental focus affected the health of telomeres. But to me, the most interesting part of what they found was that stress had a major impact on the length and health of telomeres, and that in turn had a major impact on the risk of disease.
Let’s back up a second. So what exactly are telomeres again? Sequences? It always helps me to think of telomeres as the bumpers at the ends of DNA strands. Telomeres are noncoding sequences that, for a long time, no one thought much about. They don’t make proteins and at first glance aren’t super-active in the body. But researchers discovered that they actually do serve a vital purpose: telomeres protect DNA strands, making sure that every time it is replicated by cells, the copy is true to the original. Telomeres are very sensitive to the environment, which means that, like good car bumpers, they always take the first hit. Anything biochemically harmful (like stress) is going to damage the telomeres much more than the DNA. When the telomeres are hurt, they send signals to the rest of the cell letting it know that the bumpers have taken too many hits and that the cell should respond. The cell reacts in two major ways. The first is that when the telomeres get too short (too many bad parallel-parkers in the neighborhood), the cell can become senescent, which is a science-y word for old. This means the cell retires and doesn’t do its job anymore. Take collagen (the protein in skin that makes it supple and prevents wrinkles). If too many of the fibroblast cells that are supposed to be making collagen hit the road to play shuffleboard at Del Boca Vista, you’re left looking a decade older than you actually are.
Lots of things can damage the telomeres and lead to premature cellular aging, but chronic stress is a big one. When a cell becomes old or dies, it’s not the end of the world, but if there is too much cell death in one place, it can lead to poor health. For instance, if there is too much cell death in the pancreas, you won’t be able to make enough insulin, which can lead to diabetes. The response a cell can have to damaged and shortened telomeres other than senescence is that it can become precancerous or cancerous. When that happens, it means the ability of the cell to copy its DNA correctly has been compromised, and it begins coding for mutations that say, “Keep making cells forever!” This causes the cells to replicate uncontrollably and grow into a tumor that continues to grow and grow and grow. Simply put, if there is too much damage to your telomeres and they become excessively shortened, it can lead to premature cellular aging and disease or cancer. This adds yet another fun variable to the dating game; not too far into the future, ladies might start looking for partners with long telomeres.
Research on telomeres and stress is relatively new, but we do know that early childhood adversity predicts shorter telomeres in adults, showing us the lasting imprint that early stress has on cellular aging and disease processes. Elissa Epel worked with researcher Eli Puterman and other colleagues to examine data for 4,598 men and women collected as part of the U.S. Health and Retirement Study. They assessed cumulative adversity for both childhood and adulthood by reviewing responses to health questionnaires. For childhood stressors, criteria included a participant’s family receiving help from relatives because of financial difficulties, the family relocating due to financial difficulties, a participant’s father losing his job, a parent’s substance abuse or alcohol use causing problems in the home, whether the respondent had experienced physical abuse before age eighteen, repeated a school year, or gotten in trouble with the law. The questions about adult stressors surveyed death of a spouse, death of a child, qualifying for Medicaid, experiencing a natural disaster, being wounded in combat, having a partner addicted to drugs or alcohol, being a victim of a physical attack, or having a spouse or child with a serious illness. Epel and Puterman then looked at each respondent’s telomere length. They found that while lifetime cumulative adversity significantly predicted telomere shortening, that shortening was due mostly to the adversity experienced in childhood; adult adversity on its own was not significantly associated with telomere shortening. For each childhood adversity a study participant experienced, his or her odds of having short telomeres increased by 11 percent. Epel and Puterman’s data also showed that household adversities, such as abuse or having a parent who used alcohol or drugs, were a stronger predictor of telomere shortening than household financial stress.
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.
So does that mean genes don’t matter? All you need is a mom who licks and grooms you a lot? Not so fast. While the epigenetic part of the equation is new and exciting and tells us a lot we didn’t know, there’s no discounting the impact of the DNA that comes from the good old egg and sperm. As we know, it’s all about nature and nurture. You are handing down to your kids both your genome and your epigenome and they both count in determining health. For instance, you might be blessed with some crazy-long telomeres. Maybe every woman on your mother’s side of the family has lived to be over a hundred while never looking a day over seventy-five. But during early childhood you experienced adversity, and now you have a high ACE score. Your telomeres are being chipped away at faster-than-normal rates, but because of your genetically long telomeres, you’ve got a cushion. In that case, there may not be a dramatic result; you’re not necessarily going to live to be a hundred, but you also might not see the premature mortality that your ACE score would predict. However, if you don’t have the genetic advantage of long telomeres, it could be a different story. If you go through childhood adversity, the shortening of your telomeres could lead to worse health outcomes than you might otherwise experience. And just like two siblings with the same parents might have different eye colors, they also might have different lengths of telomeres, which can lead to different outcomes even if they experience similar doses of adversity.
The research on epigenetic regulation and telomeres reinforced what I already suspected—early detection is critical. Now more than ever, I believed if we could identify those at risk for toxic stress by screening for ACEs, we had a better chance of both catching related illnesses early and treating them more effectively. Not only that, but we could also possibly prevent future illness by treating the underlying problem—a damaged stress-response system. If we put the right protocols into place in pediatric offices across the city, country, and world, we could intervene in time to walk back epigenetic damage and change long-term health outcomes for the roughly 67 percent of the population with ACEs and their children. And, someday, their great-grandchildren.
The potential for outcomes like these and the science behind them had me fired up. I had already graduated from talking people’s ears off at cocktail parties to reaching out to every well-connected person I knew in the medical community in search of someone who had more power than I did and who would commit to doing something. My own clinic had already begun instituting routine ACE screening for every patient, but there were so many other doctors out there who could benefit from this information. Having grown up in Palo Alto in the eighties back when it was closer to middle class (as opposed to straight-up wealthy like it is now), I knew that kids with ACEs live in lots of different kinds of neighborhoods. Several of my classmates at a Palo Alto high school attempted suicide when I was there, and I later heard stories of parental substance abuse and mental illness the students had struggled with in secret. Even in areas much better off than Bayview, toxic stress was essentially invisible to the health-care system.
Bayview might be a fairly obvious place to look for the impact of adversity, but toxic stress is an unseen epidemic affecting every single community. Since the original ACE Study was published, thirty-nine states and the District of Columbia have collected population ACE data. Those reporting their data show that between 55 and 62 percent of the population have experienced at least one category of ACE, and between 13 and 17 percent of the population have an ACE score of four or more. The states with the highest rates of ACEs among young children were Alabama, Indiana, Kentucky, Michigan, Mississippi, Montana, Oklahoma, and West Virginia. Left unchecked, the effects of ACEs and the toxic stress they create were being handed down by well-meaning parents in families all across the country and, undoubtedly, around the world.
After a great conversation with Dr. Martin Brotman, the CEO of California Pacific Medical Center at the time and my stalwart champion, I saw my chance. Every hospital CEO in San Francisco was part of an organization called the Hospital Council of Northern and Central California. This group came together for lots of reasons, but one of its many jobs was addressing health-care disparities in the city. Dr. Brotman helped lead the health-disparities task force within the council and was excited about what I had told him about ACEs and our work at the clinic. He immediately invited me to give a presentation about ACEs to the council. Feeling the kind of excitement that almost makes you want to throw up, I left his office that day thinking, This is it! This was my chance to go to the decision-makers and the health-care-shapers and blow the lid off this thing. I’d better not screw it up.
I spent weeks preparing for my presentation.
On the day, I knew I was ready, but as I sat in the lobby after showing up ridiculously early, I realized I hadn’t ever been this nervous, not even for my medical boards. I had just a small block of time on the CEOs’ agenda, and when I was finally shown into the room, they were all there. Mostly older men, mostly white, there were roughly twelve of them, comfortably spread out around a U-shaped table, papers stacked and strewn around their salad plates, multiple beverages stationed next to laptops. Some smiled pleasantly while others nodded. For a minute I cursed my bad luck for having gotten a slot at the end of what was obviously a very long business meeting. If I couldn’t keep them riveted, I hoped I could at least keep them awake. Dr. Brotman stood up and graciously introduced me. I shook hands with everyone and then made my way to the front of the room and popped my jump drive into the computer. After what felt like the longest thirty seconds of my life, the drive connected and I pulled up my first PowerPoint slide.
I looked up and noticed a short, heavyset Caucasian woman in the back silently clearing plates and refilling coffee. It crossed my mind briefly that I wouldn’t mind trading places with her. A tremor of self-doubt unsettled me for a moment. I took a deep breath. If this were about me, I wouldn’t even be here. No way. But this was for my patients. With that in mind, I silently exhaled and started talking. For a good twenty-five minutes I held forth, trotting out the data, the science, the biological mechanisms. Like Dr. Felitti, I was convinced that once people saw the figures, the sheer numbers of people living with the effects of ACEs, they would be blown away. I didn’t talk about my patients at all; I talked about their stress-response systems. Months of practicing my talking points at borderline socially inappropriate moments had helped me polish what I thought were my most powerful arguments.
Finally, I stopped.
I paused for a few moments, hoping to let the import of it all sink in. Then I said some approximation of “Okay, guys, so what are you going to do about it?”
I looked at their expressions, and I could tell immediately that their reaction was not going to be what I had hoped. My stomach tightened. A slow-moving burn began to make its way across my face, spreading the embarrassment cell by cell. My body may have registered it before my mind, but rapidly I knew one thing. Though it seemed they all agreed that what I had just said was both striking and important, they could clearly tell that I was profoundly naive about how things worked. What was written in their expressions was soon followed up by statements amounting to something along the lines of “Okay, Nadine, what are you going to do about it?”
Looking back on it, I realize that all I did was present them with a problem. When they asked me questions about solutions, I didn’t have good answers. They probed me about screening protocols and wanted to know what best-treatment practices were and how I thought they could be implemented. I tried my best to explain that right now there wasn’t a protocol for anything. That was why I was coming to them. Wouldn’t they figure out how to implement the best universal screening tools and come up with protocols for other doctors? That was their job, right?
Judging by the thrust of their questions, it sure wasn’t.
It became pretty clear that the CEOs weren’t going to take up this cause on their own time, despite the fact that they were supportive of it. In terms of priority, it certainly wasn’t going to jump the line ahead of seismic upgrades for their buildings or the next audit from the Joint Commission on Accreditation of Healthcare Organizations. How naive was I to think that they would just drop everything for this? I sputtered through my goodbyes, all the while feeling like a cartoon balloon, slowly and sadly deflating in the middle of the room. I don’t really remember how that meeting ended, what I said, or who sent me on my way with a kind nod and a handshake. There is still a bit of a fog about the last couple of minutes of the meeting.
Eventually, I reached the elevator and proceeded to repeatedly jam my finger against the Down button.
I had worked really hard, I had prepared, I had convinced them, but still nothing was going to come of any of this. I had been living in the world of ACEs and toxic stress so intensely for so long that it felt like the most important thing in the universe. It was straight-up weird to me that I could explain this to other doctors and they could see it too and even agree but still not jump out of their chairs. I wasn’t mad or upset at them—I was just confused. My sense of confidence in reality as I knew it was shaken, and this led me to a line of questioning I hadn’t entertained before. What if this puzzle I had put together about adversity wasn’t the five-alarm fire I thought it was? Even worse, what if there wasn’t anything we could do about it?