FOR MOST PEOPLE, the name Dr. Robert Guthrie doesn’t set their hearts aflutter, but as my brothers like to remind me, I might be a special case. In my mind, Dr. Guthrie is right up there with JFK Jr. and Idris Elba. Definitely on my short list for the “name any person, dead or alive, you most want to have dinner with” game. I don’t know if People magazine was around in 1961, but if it was, the development of newborn screening should have earned Dr. Guthrie a spot on the cover of the “Sexiest Man Alive” issue.
I first heard of him when I was a young medical student learning about newborn screening, which is an important way for doctors to identify a long list of life-threatening diseases like hypothyroidism and sickle cell anemia. Anyone who has had a baby may remember that at some point, after about twenty-four hours, the baby’s heel gets poked and a drop of blood is collected so the lab can do what’s called a newborn screen. This test allows doctors to identify disorders (like hypothyroidism) long before symptoms develop and then treat the underlying issue before it can cause problems. This leads to much better outcomes for patients, and it’s now the standard of care in every developed country around the globe. But that wasn’t always the case.
Dr. Guthrie started his career as a cancer researcher, but his life changed in 1947 when he and his wife, Margaret, had their second child, a son they named John. Not long after John was born it became clear that he had a significant mental disability, what was referred to at the time as “mental retardation.” Despite taking him to specialist after specialist, the Guthries never learned the cause of John’s disability. After his son was born, Guthrie dedicated himself to the prevention of mental disabilities. By 1957, he had become the vice president of the Buffalo chapter of the New York State Association for Retarded Children. The following year, Margaret Guthrie’s sister, Mary Lou Doll, had a baby girl whom she named Margaret after her beloved sis. At first, Margaret was the picture of a happy infant, doing all of the smiling and cooing that the books tell you to expect. But over time, baby Margaret’s demeanor changed. She became quieter and less interactive, and by seven months, she began losing her milestones and developed an odd habit of dropping her head. Concerned, Mary Lou Doll took her daughter to her pediatrician, who diagnosed Margaret’s “head dropping” as seizures and determined her to be “somewhat retarded.” Although there was a test available at that time for the rare genetic disease phenylketonuria (PKU), it wasn’t done. The pediatrician did, however, recommend a brain wave test, although he said there was no hurry “as she was very young for specific results.”
It wasn’t until Margaret was a year old that Mary Lou conferred with her brother-in-law about her daughter. He suggested she take the baby to the University of Minnesota, where she was finally tested and diagnosed with PKU. Phenylketonuria is caused by an enzyme deficiency that renders the body unable to metabolize phenylalanine, an amino acid found in most proteins, including breast milk and baby formula. Over time, a byproduct of phenylalanine builds up in the body and slowly poisons the developing brain and nervous system. Margaret Doll’s seizures were a result of a toxic buildup of this phenylalanine byproduct. There is a treatment for PKU, but here’s the kicker—it isn’t a million-dollar-a-dose medicine or some fancy implantable medical device. To prevent the neurotoxicity of PKU in a child, all you have to do is stop feeding the kid anything with phenylalanine in it. If you’ve ever read the fine print on a can of diet soda, you might have wondered why it says “This product contains phenylalanine.” That piece of information is meant to help people with PKU maintain the phenylalanine-free diet that is so critical to their health.
Margaret Doll was started on a phenylalanine-free diet when she was thirteen months old, and over time she regained some of her developmental milestones. She sat up at eighteen months and began walking when she was two and a half years old, but she remained severely intellectually disabled, with psychologists reporting her IQ as twenty-five.
The combined heartbreak from his son and his niece made Dr. Robert Guthrie a man on a mission. He knew that if the PKU was caught early enough, the phenylalanine-restricted diet would prevent severe neurological damage. At the time, PKU was diagnosed by what was called the diaper test, which involved testing for the toxic phenylalanine byproducts in the urine. Though the test was accurate, it was not sensitive enough to detect the toxic byproduct until after severe brain damage had already occurred.
Guthrie took it upon himself to find a better method of measuring blood phenylalanine. Borrowing methods from his experience in cancer research, he was able to devise a test that required only a few drops of blood. The blood was placed on a piece of filter paper, then the filter paper was put in a culture of bacteria that would grow only in the presence of phenylalanine. If bacteria grew, he knew there was phenylalanine where there shouldn’t be.
In 1960, one of the first trials of the Guthrie test was done on children at the Newark State School for the Mentally Retarded. The test confirmed every single known case of PKU as well as four that had gone undetected. Soon after, Guthrie set up a laboratory near the Buffalo Children’s Hospital, and over two years he went on to test more than four hundred thousand infants from twenty-nine states for PKU. The new screening method identified thirty-nine cases of PKU in newborns, and treatment was started early enough to prevent brain damage. Further, the test didn’t miss a single case of PKU.
For years after he developed the test, Guthrie was a vocal advocate of screening all newborns for PKU before they left the hospital. He fought side by side with like-minded organizations to demand that the test be mandated by law. He succeeded, and eventually the newborn screening test was expanded even further; it now identifies more than twenty-nine conditions that can lead to long-term neurologic damage. The Guthrie test has been used in more than seventy countries and is responsible for helping countless children reach their God-given potential. Now, if that doesn’t earn you the “Sexiest Man Alive” title, I honestly can’t imagine what does.
To me, Guthrie’s true legacy was that he set the precedent for universal screening. It’s something I think about every time I see an ACE score in a patient’s chart. In the same way that babies with PKU aren’t born with any outward signs that they have the genetic disorder, kids don’t come into my office with signs around their necks saying I HAVE TOXIC STRESS. That’s why the universal is just as important as the screening. Time and again, I am reminded of what Guthrie showed the world—that we shouldn’t wait for our kids to come to us with symptoms of neurologic damage when there’s something simple that can be done to prevent it.
Three years after we opened the Center for Youth Wellness, I began seeing a new patient who brought Guthrie’s lesson home yet again. Lila was two and a half years old, blond, bubbly, and precocious. One day in the fall of 2015 I sat at the conference table with my colleagues sipping tea and reviewing her chart. Once a week CYW has multidisciplinary rounds; that’s where we discuss treatment plans for patients who have been identified by the clinic as being at high risk for toxic stress. This approach to care was something that started in the Bayview clinic out of necessity.
In the early days of the Bayview clinic, I was overwhelmed not by the workload (although that was some craziness too), but by the dire situations my patients and their families were often in. I was trained to treat asthma and infections, but my patients needed so much more than prescriptions for inhalers and antibiotics. Sometimes they needed housing, protection from abusive parents, or even things as simple as basic toiletries. One day I had a patient’s dad tell me that his family had been thoroughly burglarized; the person who broke in had even taken the toilet paper off the roll. (You know you have been good and robbed when someone takes your freaking toilet paper.) That same dad proceeded to board up the windows to prevent another break-in. Soon after, all three of his children came to me on the same day with severe asthma exacerbations, and the dad asked, sincerely, “Hey, Doc, do you think it’s bad for their lungs that we’re smoking meth in the house with all the windows boarded up?”
That same week, a seven-year-old patient was brought to me with a complaint of chronic headaches. She had just been removed from her uncle’s home, a studio apartment where she had literally watched her uncle sexually abuse her fifteen-year-old cousin, his daughter.
Back then I dictated my notes into a tape recorder, and when I listen to them now, I swear my heart remembers, aching yet again with grief for my tiny patients. There were days I would walk out of the exam room, close my office door, lay my head down on my desk, and just cry. And I definitely wasn’t the only one. At lunch or after work, I would find myself talking about my patients to Dr. Clarke and our social worker Cynthia Williams, partially to blow off steam but also because talking to one another helped. We would put our heads together to find avenues of support for our patients, which was good for them and for us.
Eventually, I realized that what we were doing at the clinic was an informal version of a practice I had learned on the oncology ward at Stanford, referred to as multidisciplinary rounds. In the pediatric oncology unit, there are understandably some really high-needs patients. Every week a group would meet that included the head oncologist, the social worker, the therapist, the child-life specialist (someone who helps kids through painful procedures), and a nephrologist (kidney doctor) or whatever specialists were needed for that particular case.
It was a perfect example of divide and conquer. When you’re caring for kids with cancer, by definition you have an incredibly sensitive and complex situation—of course no one person (doctor or otherwise) can adequately address all of those needs. When I thought about our patients at the Bayview clinic, their needs didn’t seem too different in terms of complexity of care. So instead of bellyaching in the break room, Cynthia Williams, Dr. Clarke, and I began meeting every week, bringing a stack of charts to review and calling it, Stanford-style, MDR.
Straight out of the gate, we could all feel that the practice made a huge difference. It allowed me to do my job well without having to split my energy or wear multiple hats. I knew when I walked into an exam room that I would have a place to bring all of the challenging issues at home that were also affecting my patients’ health. I didn’t need to be a social worker or a therapist; I could let Williams and Dr. Clarke do their jobs in a way that coordinated with what I was doing in the exam room. As a result, my patients got a better doctor, and their additional needs were addressed by someone who was trained to take care of them.
We weren’t aware of this at the time, but our approach would later become a best practice known as team-based care. Our patients’ lives didn’t get less complicated, but we found that this new model helped patients get better faster, and it had the added bonus of improving staff morale (especially mine). It was such a success that when we opened CYW, it was an important priority to carry that practice forward.
Years later, as I looked around the table at CYW, I felt a sense of pride and confidence seeing two social workers, a psychiatrist, a clinical psychologist, a nurse practitioner, and two wellness coordinators whose job was to manage the interlocking web of patient treatment plans across disciplines. I was about to give all of them the scoop on what turned out to be my most unexpected patient in months, and I knew that together we could help her.
When Lila first came into my exam room, she was just tagging along with her baby brother, Jack, who was there for a follow-up appointment after a trip to the ED for an ear infection and a bad cold. It was the third ear infection for the nine-month-old and he had also had two bouts of pneumonia. His parents wanted to make sure that this cold wouldn’t “turn into” another pneumonia. Lila was the same age as my son Kingston (yep, managed to find a husband and have a baby in the middle of all this). I laughed as she scampered around the exam room and asked precocious questions, just like Kingston did every morning as I was getting him dressed.
The family was new to the area, having just moved to the Bay Area from Ohio, so once I checked the ear (it was fine) and listened to his lungs (all clear), we scheduled physicals for both Lila and her brother. The family was freaking adorable. I see a lot of beautiful families in my line of work, but these guys really stood out. Molly and Ryan were young parents, but completely doting and caring, and to me they seemed as close-knit as the Cleavers. In the course of my exam, I encountered a soiled diaper (occupational hazard), and Ryan jumped up to change it, apologizing profusely. It was sweet to see both parents so hands-on with the kids.
Two weeks later when I saw that both kids were on my schedule for their physicals, I smiled instantly. I was looking forward to seeing them again. I walked into the room and reviewed all of the standard intake and medical-history forms. I was glad to see that Jack had no new symptoms and noted that Molly’s only concern was Lila’s growth. Ryan wasn’t able to make the visit, so it was up to Molly to explain her daughter’s history. She told me that when Lila was born, she was at the twenty-fifth percentile for height and weight, but over the subsequent six or so months, she had drifted down below the third percentile and stayed there. Their previous pediatrician had counseled them about diet and even recommended PediaSure (a nutritional supplement), but nothing seemed to work. Molly didn’t understand why Lila was so small. Both she and Ryan were average height and Lila had never had any chronic health problems. As I sat down with her to finish reviewing the medical-history forms, I flipped to the ACE score and had to force myself not to do a double take.
Maybe Mom misunderstood the directions? I thought. Maybe she wrote down her own ACE score instead of the kids’. According to the paperwork, Lila had an ACE score of seven and her nine-month-old brother’s score was five.
I started my usual spiel, figuring Molly would realize her mistake: “New research has shown that children’s exposure to stressful or traumatic events can lead to increased risk of health and developmental problems, like asthma and learning difficulties. As a result, at this clinic we now screen all of our patients for adverse childhood experiences. I’m going to review this list of ten items, and you don’t have to tell us which ones your child experienced, only how many. I’d like to take a moment to go over your responses.” Molly was nodding her head the whole time.
“I totally believe it,” she said.
“So you’ve heard of ACEs before?” I asked, a little perplexed.
“No, but when I read about it on the piece of paper, it made total sense.”
She confirmed that her kids’ ACE scores really were seven and five.
So she hadn’t filled out the form wrong.
The realization knocked me in the gut. I see patients with high ACE scores, even some that are pretty young, every day, and it’s always tough. But Lila’s mannerisms reminded me so much of my own son’s that her ACE score hit me in a way that I hadn’t anticipated. The doctor in me was grateful to get the insight into what might be going on with her health, but as a mother, it made my stomach sink. I wanted to throw my arms around Lila, hold her tight to my chest, and tell her it would be okay. I wanted to make those seven ACEs disappear like kissing away one of Kingston’s boo-boos. But I couldn’t. And it wasn’t my role. What I could do was make sure that Lila’s ACEs weren’t written into her biology for the rest of her life. In fact, that was my job.
I knew from Lila’s ACE score that she was at much greater risk for a host of adult health problems than other kids. But what did this information mean for how I should do my day-to-day job? Felitti and Anda had looked at health outcomes in adults, but Lila was unlikely to face most of those diseases for decades to come. Fortunately, our research team at CYW had made good progress in filling in some of those blanks.
Our team reviewed over sixteen thousand research articles on the impact of childhood adversity on health. What we found was that childhood adversity is associated with a variety of diseases and conditions in children that can be observed as early as infancy. In babies, exposure to ACEs is associated with growth delay, cognitive delay, and sleep disruption. School-age children show higher rates of asthma and poorer response to asthma rescue medication (such as albuterol), greater rates of infection (such as viral infections, ear infections, and pneumonia), and more learning difficulties and behavioral problems, and adolescents exhibit higher rates of obesity, bullying, violence, smoking, teen pregnancy, teen paternity, and other risky behaviors such as early sexual activity.
I sat down to walk Molly through what I suspected was going on with her daughter’s health.
“I think that because of what Lila has experienced, her body may be making more stress hormones than it should, and this may be affecting her growth,” I said.
This seemed to make intuitive sense to Molly.
“Yeah. We were working on her weight with her previous pediatrician. Her dad had times when he would be away from the house, and it seemed like when he was away, her weight would pick up a little bit, but when he came back, it would fall off again. There has definitely been a lot of stress in our house.”
“Wow. Did you ever mention this to her previous doctor?”
“No,” she replied. “He never asked.”
If it wasn’t for the ACE scores, no one would have suspected that Lila and her brother were at such high risk for so many health and developmental problems. Possibly they might have gotten some attention if they’d started to show behavioral problems in preschool, but even in that case, it’s likely they would have been diagnosed with ADHD and been funneled down the medication path. If they had never manifested any behavioral symptoms, chances are—even if they developed asthma, or an autoimmune disease, or any of the other significant immunological consequences of toxic stress—the underlying problem would likely have gone undetected and untreated. Guthrie had shown that the only way to radically move the needle on patient outcomes is to screen universally, because otherwise you are relying on chance: The chance that Lila’s symptoms would get bad enough that her doctor asked more questions. The chance that this particular doctor had heard about ACEs and knew to ask those questions in the first place. How much damage could be done while you were waiting for the right questions to be asked, the right tests to be run? Guthrie knew. His sister-in-law knew. They saw what happened when PKU was not tested across the board, when the opportunity for early intervention was lost. That is why an ounce of screening is better than a pound of cure.
In the case of PKU, it’s clear that early intervention is needed to treat the condition successfully, but what about ACEs and toxic stress? It’s actually just as clear. All the science about the development of the neuro-endocrine-immune system tells us one thing: intervening earlier is better (and I mean way, way, way better). That’s not to say that older kids and adults with ACEs can’t benefit from interventions (more on that to come), but the later we start, the more intensive (and expensive) the treatment has to be and the less likely it is to be effective. The reason for this is that starting earlier gives us more tools to work with.
The past several decades of neuroscience research explains why early adversity has such an outsize impact on children’s development. The prenatal and early childhood periods offer special windows of opportunity because they represent “critical and sensitive periods” of development. A critical period is a time in development when the presence or absence of an experience results in irreversible changes. Much of what we know about critical periods comes from research on binocular vision (the ability to perceive depth and create a 3-D image out of inputs from both eyes). When a baby is born with eyes that are misaligned (with crossed eyes or a lazy eye), the brain will have trouble creating a coherent 3-D image and depth perception is impaired. But if the misalignment is identified and corrected by age seven or eight, the child can go on to develop normal binocular vision. After age eight, however, the window closes and the opportunity for normal 3-D vision is permanently lost. (Or so we thought—new data suggests that the window for binocular vision may be longer than previously believed, and exciting research is focused on learning if we can re-open windows previously thought to be closed.) Since the discovery of critical periods in the brain’s visual cortex, scientists have found that numerous other brain circuits demonstrate critical periods as well.
A sensitive period is a time when the brain is particularly responsive to a stimulus in the environment, but unlike critical periods, the window doesn’t totally close at the end of the sensitive period; it just gets a lot smaller. The development of language is a great example of a neural circuit that demonstrates a sensitive period. Everyone knows that it’s way easier to learn new languages when you’re a kid than when you’re an adult. I have some European friends whose kids speak four languages fluently—English, French, German, and Spanish—each with a flawless accent. Meanwhile, several years and hundreds of dollars on Rosetta Stone later, my French is très terrible.
Critical and sensitive periods are times of maximal neuroplasticity (the brain’s ability to rewire or reorganize itself in response to a stimulus). This growing and changing of neurons and synapses can happen in response to injury, exercise, hormones, emotion, learning, and even thinking. Our brains are always changing in response to our experiences, and overall, that’s a good thing.
There are two types of neuroplasticity, cellular and synaptic. Synaptic plasticity is a change in the strength of the connection across the junction from one brain cell to the next (the synapse). It’s kind of like changing your voice from a whisper to a shout. Cellular plasticity, however, is a change in the number of brain cells that are talking to each other, the difference between one person shouting and a whole stadium shouting. While synaptic plasticity is lifelong (it’s how an old dog learns new tricks), cellular plasticity happens most rapidly in the first years of life. About 90 percent occurs by the time a child turns six, but the rest of it stretches out until about age twenty-five.
The way brain development works is like those weird topiary bushes that grow in the shape of Mickey Mouse or a giant dinosaur (stay with me here for a second). Obviously, they don’t just grow that way on their own; they are pruned. Babies are born with an oversupply of brain cells and the brain also goes through a pruning process. The brain cells on the circuits you don’t use get pruned, and the ones on the circuits that you do use grow and strengthen. Our experiences, both positive and harmful, determine which brain pathways are activated and continue to strengthen over time. In that sense, early experiences literally shape the brain.
We know that early adversity activates the brain pathways that are associated with vigilance, poor impulse control, increased fear, and inhibition of executive functioning. But if we can identify kids who are at high risk for toxic stress early enough, we can intervene in time to take advantage of high levels of both synaptic and cellular plasticity. The most effective way to rewire the brain is to implement early interventions that help to prevent the stress response from becoming dysregulated and that support practices that buffer the stress response (as with child-parent psychotherapy). By doing this, you give the brain the greatest opportunity to grow in new and healthy ways.
So what about all of us old dogs? Well, when it comes to learning new tricks, the good news is that the hormonal changes occurring in adolescence, pregnancy, and new parenthood open up windows of neuroplasticity that are believed to be additional sensitive periods. Testosterone (in boys) and estrogen and progesterone (in girls) are sex hormones that lead to all of the mortification associated with adolescence (acne, body hair, breasts, menstrual cycles). Another important hormone is oxytocin, a powerful bonding hormone that is released in very high levels by the mother during childbirth and in the immediate postpartum period. All of these hormones stimulate synaptic plasticity, biochemically enhancing the ability to learn and adapt to one’s environment. These times represent special opportunities for healing, moments when enriching experiences have an even better shot at being “wired in.”
More good news—there are things that you can actually do yourself to boost your synaptic plasticity; sleep, exercise, nutrition, and meditation all enhance the process. That being said, a little more patience and consistent practice is required for adults, since the change will not be as radical or as fast as it is in young children. We know that the earlier we start, the more tools we have—young children are the most vulnerable to adversity, but they also have the greatest capacity for healing when the interventions are begun early. And we also know that it’s never too late to use biology to our advantage for healing.
Guthrie famously developed the simplified blood phenylalanine test in three days. Unfortunately for us at the clinic, developing a fast and easy screening protocol for ACEs was anything but fast and easy. By 2015, we’d been working on it in one way or another since 2008. At the Bayview clinic we started by simply asking about patients’ history concerning the ten ACEs and recording that information in their medical charts. The problem with this approach was that it took a long time and sometimes meant that the doctor asking the questions had to navigate a serious emotional obstacle course that most primary-care clinicians have neither the time nor the training to navigate thoughtfully. Though it helped us provide better care for our patients, it wasn’t ideal. We knew we had to make some adjustments if it was going to work for doctors outside our own little clinic.
The great thing about CYW is that it is built on the successes of the Bayview clinic. We were on the right track in terms of screening, and once CYW had the resources, our clinical and research teams put their heads together to refine the screening tool so it could work for every doctor. It needed to be simple to use and evidence-based.
Fast-forward a few years (not to mention some sweat and tears, but fortunately no blood). The screening tool that Lila’s mom filled out was much different than the one I’d first used with my patients. First, the new one was on paper (or a tablet), something that a parent was able to fill out before I came into the exam room. Second (and this was the real innovation), on the new one, we listed the ten ACEs and specifically asked the patient’s parents not to tell us which of them their child had experienced, only how many. At the bottom of the page, the caregiver wrote the total number, and that’s the ACE score. We call this our “de-identified” screen because it doesn’t identify the individual ACEs, and it goes a long way to solving two of the biggest challenges—time (previously, a positive screen took a very long time to unpack) and the sensitive information we’re asking for. As both Dr. Felitti and I had seen firsthand, doctors, more than patients, are hesitant to get into conversations about past incidences of abuse or neglect. They worry their patients will be uncomfortable, that they won’t tell them the truth, or, worse, that they will tell them the truth and the visit will be derailed with an emotional outpouring or the need to file a report with Child Protective Services. The de-identified screening tool takes all of these concerns out of the equation.
The other important thing that the CYW ACE questionnaire did was go beyond the traditional criteria develop ed by Felitti and Anda and ask about additional risk factors for toxic stress. We don’t call them ACEs because they are not from the ACE Study and we don’t have the large body of population data to tell us odds of disease, but our experience in Bayview told us that our patients faced other adversities that repeatedly activated their stress-response systems. Our research team worked actively with the community (youth and adults) to learn what the greatest stressors were in their day-to-day lives. Informed by these insights, we reworked our screening tool to include other factors that we believe may also increase the risk for toxic stress.
Community violence
Homelessness
Discrimination
Foster care
Bullying
Repeated medical procedures or life-threatening illness
Death of caregiver
Loss of caregiver due to deportation or migration
In our teen screener, we also include the following:
Verbal or physical violence from a romantic partner
Youth incarceration
We score these supplemental categories separately so that we don’t lose the ability to apply findings from the scientific literature. I know from the ACE Study that if a patient has an ACE score of four or more using Felitti and Anda’s criteria, he is twice as likely to develop heart disease and four and a half times as likely to become depressed. Researchers are just beginning to look at the supplemental categories on a large scale, but the preliminary data indicates that stressors at the household level (the traditional ACEs) seem to have a greater effect on health than stressors at the community level. This was a surprise to many in the field (myself included), but the data suggests that if a child grows up in a stressful community environment but has a well-supported and healthy caregiver, he or she is much more likely to stay in the tolerable stress zone as opposed to the toxic stress zone.
When I reviewed Lila’s screen, all I saw was that her score was a seven plus zero (seven for the traditional ACE score and zero for our supplemental score). That was enough information to tell me what I needed to do next. Molly didn’t have to disclose any of the details of what had happened in their family if she didn’t want to. And for the most part, she didn’t. She mentioned only that Ryan had spent some time in rehab and that he had a history of ACEs himself. As I looked at Lila’s ACE score, part of me wanted to know the whole backstory. I wanted to know how this dad who had been so happy to jump on a dirty diaper might be harmful. I wanted to know about this mom and what her story was. But to do my job well, I couldn’t be the one to unpack that. In order to make sure that my twelve other kids on the docket for the afternoon were also screened for ACEs, I had to trust my team to take it from here. The de-identified screen allowed me to recognize that Lila’s failure to thrive was most likely due to toxic stress. I needed only to get her the right care in a way that was fast and easy enough that I could reliably do it for every single one of my kids without being in the clinic until midnight every night.
I brought Lila’s case to multidisciplinary rounds with a recommendation that she start child-parent psychotherapy. Ultimately, Molly would be best served by getting into the nitty-gritty of her daughter’s ACE score with Dr. Adam Moss, Alicia Lieberman’s most recent postdoctoral fellow. Her treatment involved three simple steps. The first and most critical was simply helping Molly better understand the problem and what we could do about it—going a little deeper into how stress hormones affected growth and how Molly herself had the innate capacity to be a buffer for her daughter’s stress response. To make that happen, we had to help Molly learn how to get her own stress response in good working order. We explained to her later that we had a specialist who would teach her how to be a healthy buffer for her child’s stress. The second step was getting mother and daughter plugged in to CPP, and the third step was just good old-fashioned PediaSure, which I thought would be more effective once we had dealt with the underlying toxic stress. Within three months, Lila was back on the growth curve.
When I think back to the early days of Diego and how overwhelmed I felt before we began the team-based approach, I knew this was a better way for everyone. Now, seven years later, it felt like this was how it had always been. It just made so much sense.
Unfortunately, sometimes what makes sense doesn’t always align with the reality of medical practice. Another badass medical “she-ro” of mine is Sue Sheridan. While she is not a medical doctor, like Guthrie she has a son with a severe disability that inspired her to work tirelessly on behalf of families like hers. Most people have either had or know of a baby who was born with jaundice, a condition in which the infant’s skin and eyes appear yellow. You might have even seen a picture or two of a friend’s baby under the phototherapy lights, looking like he is in the newborn equivalent of a tanning bed.
Over 60 percent of newborns develop some amount of jaundice. The signature yellow skin lets pediatricians know that there is a buildup of a chemical called bilirubin in the baby’s system. Bilirubin is created when the body breaks down old red blood cells. It is naturally processed by the liver and excreted by the body (which is actually why your pee is yellow). But when babies are born, it takes a little while for their livers to come online and function to full capacity, so the bilirubin can build up. Bilirubin is typically harmless, but if the levels get too high, it can cross the blood-brain barrier and cause brain damage.
When Sue Sheridan’s son Cal was first born, he appeared as healthy and beautiful as a baby could be. But within the first twenty-four hours of Cal’s life, his skin started to turn yellow. Sue and her husband were told not to worry, as jaundice was quite common in infants. No bilirubin test was done. At the time, standard of care was to do a visual inspection, meaning the pediatrician would eyeball the patient and decide if the jaundice looked severe enough to treat. Even though a blood test existed to measure bilirubin levels, it wasn’t used routinely. The following day, Cal’s yellow color continued to deepen, and though the Sheridans again expressed concern, still, no test was done. When Cal was discharged at thirty-six hours of life, he was described as having jaundice from head to toe, but his parents were simply given a pamphlet as they left the hospital that suggested putting the baby near a window for sunlight. Nowhere in the pamphlet did it say that jaundice could lead to brain damage.
The day after Cal returned home, he became lethargic and started to have trouble nursing. Alarmed, Sheridan brought him in to see the pediatrician, but still no test was done and they were sent home yet again. Another day passed and Cal only got worse. Finally, he was admitted to the hospital and started on phototherapy. However, the treatment of Cal’s jaundice didn’t begin until it was too late. On the sixth day of his life, in his mother’s arms, Cal stiffened, arched his neck, and let out a high-pitched cry. Later Sheridan would learn that Cal had displayed all of the classic signs of kernicterus, a condition that occurs when bilirubin gets too high and crosses the blood-brain barrier, leading to severe brain damage. Sheridan literally watched as her baby’s brain was being overcome by neurotoxicity that could have been prevented. It was an experience that would haunt her for the rest of her life.
Although rare, kernicterus is devastating. It can result in a range of irreversible neurological damage, and for Cal, the disorder meant that he developed cerebral palsy, hearing loss, crossed eyes, and speech impairment, among other abnormalities, and would need care for the rest of his life. As if that weren’t enough to deal with as a new mom, what really ate Sheridan alive was that it hadn’t had to be that way. Through a series of tragic lapses in medical care, the urgency of Cal’s condition wasn’t recognized until the damage was done.
Years later when Sheridan’s daughter was born with jaundice, she was quickly tested and successfully treated with phototherapy. When Sheridan saw how easy it could have been to prevent Cal from numerous disabilities, she cried, feeling devastated all over again for her son. But then she got to work. She hit the road to campaign for universal bilirubin screening, something that could be added to the routine newborn care for about a dollar. She spoke at conferences, testified in front of health-care agencies, and formed a nonprofit with other mothers whose kids had kernicterus. To most people who hear Sheridan’s story, the answer seems obvious: Do the damn test. Make it mandatory. Of course! But while she was able to make a lot of progress with certain commissions and health-care organizations, she also got a huge amount of pushback from the medical community.
The doctors and heads of committees that make up guidelines for medical screenings were upset that she was trying to change practice based on “emotional stories.” Kernicterus was rare enough, they argued, that you shouldn’t alarm new parents, who already have so much on their plates. And you shouldn’t second-guess doctors. As a patient-safety advocate, Sheridan came up against a number of obstacles that seemed to be more about objections to changing the medical culture than objections to the science. For Sheridan and her son, care reliant on something as subjective as a visual inspection had had disastrous consequences, and she was determined to make sure more kids weren’t harmed for lack of a simple screening test. Sheridan’s campaign succeeded in putting kernicterus front and center on doctors’ radars. She got the Centers for Disease Control to issue an alert to hospitals about the rise in cases, and she convinced the Hospital Corporation of America, a major hospital chain, to require all newborns be tested before discharge. Thanks in part to Sue Sheridan, in 2004 the American Academy of Pediatrics officially recommended that every child have a bilirubin screen in the first twenty-four hours of life.
As someone deeply embedded in medical culture, I know there is often a lot of resistance to changing practice guidelines, and much of that resistance is warranted. That’s why before CYW took steps to share our screening tool, we wanted to put some feelers out there and have a good listen. By talking to colleagues, we learned some valuable information about the potential difficulties of implementing a screening protocol for ACEs. There were some thoughtful concerns and questions, but there was also some good old stubborn resistance to implementing another screening protocol.
I get the fact that doctors can’t screen for everything. Like most of my colleagues, I find fifteen minutes to be a laughable amount of time to accomplish all of the things a pediatrician has to do in a well-child exam. In that time, we have to look at height and weight, vision and hearing, and growth and development and ask about eating, sleeping, peeing, pooping, screen time, and the dozens of household hazards ranging from peeling lead paint to unsecured firearms. And that’s before I even pull out my stethoscope. After about my second patient of the day, I find myself starting every visit with “I’m so sorry you’ve been waiting.”
Our team’s response to all of those concerns was to develop a protocol that could be completed in three minutes or less. We recognized that it was important not only to recommend to doctors that they screen, but also to help them understand why they should screen, how to screen, and what to do when they detected ACEs. So we decided to pull together a user guide that would go along with the screening tool and answer all those questions.
Around the time that I was seeing Lila, we made our screening protocol available for free online. We knew that getting folks to do things differently was really hard, which was why we set the goal for one thousand downloads over the next three years. To my surprise and our collective delight, over twelve hundred clinics and practitioners in fifteen countries downloaded the tool in just one year, blowing past our goal. When our team reached out to a focus group of doctors who had started screening for ACEs, they all said that they would never go back to not screening. It’s like a bell you can’t unring.
Building on the positive feedback we got from making our tool available to doctors, we went a step further, creating a network for pediatricians around the country to learn together about how to screen, what to do with a positive screen, and how to advance the care of children with toxic stress faster. It’s my hope that our National Pediatric Practice Community on ACEs will bring us closer to the day when ACE screening is a universal part of health care. I believe in my core that we will get there.
I’ve seen what a difference early identification and early intervention has made for my patients with ACEs, and like Robert Guthrie and Sue Sheridan, I am on a mission to ensure every kid across the country has the same chance at successful treatment. No matter where the impetus for change comes from—a doctor, a patient, a mother, a tragedy—the important thing is that patients get better care. We have to continue to refine the protocols, catch problems early, and treat our most vulnerable patients with everything we’ve got.