The Orphans of Davenport

by Marilyn Brookwood

  When a 1997 White House conference on young children’s development and learning increased public interest about early brain development, the John D. and Catherine T. MacArthur Foundation became curious. This led to conversations with Nelson and colleagues Nathan A. Fox, a University of Maryland psychologist, and Charles H. Zeanah, a psychiatrist at Tulane University, all of whom had concerns about the harm to Romanian children that Johnson had reported. Zeanah had found similar severe effects in some neglected American children, so starved for adult attention they approached and befriended random strangers.16 (Skeels and Skodak had reported similar behaviors in Davenport residents.) The next year the MacArthur Foundation launched its Network on Early Experience and Brain Development, with Nelson as director.

  To translate their concern into action, Nelson and his colleagues established the Bucharest Early Intervention Project (BEIP), a study conceived as both a scientific and humanitarian undertaking. Sponsored by MacArthur, the BEIP would ask two essential questions: what are the effects of institutionalization on brain development, and would living with families reverse those effects? Utilizing the method of a randomized controlled trial, the investigation would test three hypotheses:

  Compared with children who lived in institutions, children who lived with families would have better developmental outcomes.

  The longer children lived in institutions, the more their development became compromised.

  The age of placement into foster care could be more important than the length of time spent in foster care.17

  At the time of the study, fostering children was not an accepted method of childcare in Romania, and Bucharest, a city of 2 million, had only one approved foster family. This meant the BEIP would have to establish its own foster care program. With Tabacaru’s help, the scientists received government permission to establish Romania’s first such network. Eventually, Tabacaru established a Romanian foster care system that relegated institutionalizations to a last resort.18

  Because American foster care is temporary, the establishment of foster care in Romania meant creating an entirely different system than the one the researchers were accustomed to. In the United States, children remain with their foster families for eighteen months, although there can be frequent placement changes. At the end of that time, children either return to their parents or are released to agencies for adoption. In the BEIP model, foster care would continue indefinitely, and no child who had been fostered would ever be returned to an institution. Social workers helped the Romanian foster parents establish warm relationships and provided psychological as well as material support. Foster parents were encouraged to “care about . . . the children as if they were their own.”19 Several of the fostered children were later adopted by their foster families.

  An essential feature of the study would be comparisons of the brain development of the children who experienced foster care with those who remained in institutional care, a contrast not previously studied. To accomplish this, the investigators assembled a well-equipped laboratory in Bucharest. With the use of electroencephalogram (EEG) and event-related potential (ERP) technology, scientists planned to study electrical patterns in the children’s brains to assess neurological, cognitive, and behavioral development. Eventually, researchers also employed magnetic resonance imaging (MRI) to analyze brain differences between the groups.

  Another feature of the BEIP research protocol also set it apart from previous studies. It would be the first comparison of adopted and institutionalized children in which subjects would be randomly selected. Children would be assigned by chance to live either in a home with a nurturing foster family or to remain in an institution. That the study’s design left children in facilities known to be neglectful and even abusive raised sharp ethical questions. There were two principal reasons why BEIP scientists nonetheless went forward. First, they believed that strict randomization could dispel the suspicion raised by every previous adoption study that results favoring adoption had been contaminated by selective placement bias. Critics might ask whether children had been chosen for adoption because they had qualities that made them more desirable—perhaps they appeared healthier or more attractive, livelier or more intelligent.20 If so, adoptees’ superior outcomes might indicate some genetic advantage rather than their adoptive parents’ nurturing. In Romania and many other nations, suspicion regarding selective placement bias was supported by another cultural assumption: that children in institutions were somehow defective.21 After all, why else would they be there? A truly random selection of children would refute such suspicions.

  Second, the investigators hoped to combat Romania’s entrenched policies of child institutionalization. If the BEIP’s methods demonstrated that family environments achieved significantly better outcomes, the government might be persuaded to direct orphans toward foster care and adoption rather than into the state’s inadequate facilities. In the words of BEIP scientist Charles Zeanah, a randomized study might “benefit the larger society rather than each individual participant.”22

  When early results indicating the benefits of foster care were provided to Bucharest officials, they began to remove children from institutions. By the end of the study, only 13.6 percent of the BEIP’s institutional group children remained. The others had been adopted, transferred to newly established government foster care, or returned to their parents. Ultimately, the BEIP resulted in better conditions for a large majority of the children in both the experimental and control groups.

  After assessments ruled out children who had obvious medical problems, 136 institutionalized babies and toddlers from 6 to 31 months, who lived in six different Bucharest institutions, were selected for the study. Half the children were assigned to remain in their institutions and the other half were transferred to homes where foster parents awaited them, for many the first such caring encounters of their lives. A third group of children who had never been institutionalized was selected for comparison.23

  The BEIP’s longitudinal study began in the fall of 2000 and ended in 2005, although the participants are being followed even today. The results were remarkable, though not surprising in light of what Skodak, Skeels, and their colleagues had found long before. The three groups showed distinct differences in development, intelligence, and attachment to caregivers. At 42 months, the children were evaluated using the Bayley Scales of Infant Development II (BSID II), an assessment analogous to an IQ test. The BEIP scientists found that the mean developmental quotient (DQ) for the institutionalized group was 77.1; for the foster care group, it was 85.7; and for children who had never been institutionalized, it was 103.4 (average scores ranged from 90 to 110). A year later, when the children were 54 months, the researchers assessed them using the standardized Weschler Preschool and Primary Scale of Intelligence (WPPSI). They found that the institutional group’s mean IQ was 73.3; the mean score for the foster care group was 81.0; and the mean for those never institutionalized was 109.3.24

  The researchers discovered that the age the children entered foster care dramatically influenced their development. Just as Marie Skodak had found in Davenport’s orphans, without exception the BEIP results showed that the earlier the children had been placed, the higher their scores. Those fostered before 18 months had a mean DQ test score of 94.4 and a mean IQ score of 84.8. Those who entered after 30 months had a mean DQ score of 79.7 and a mean IQ score of 71.5. The evidence was clear: earlier intervention was not just a little better; it significantly enhanced outcomes.25

  The test results yielded yet another striking difference in children’s age-related scores. Children who entered foster care at younger ages, when they were between 19 and 24 months, had a mean developmental quotient of 89.0, but those who entered between 24 and 30 months had a mean DQ score of 80.1. The better performance of the earlier entrants suggests the effect of “sensitive periods” in early development—periods when evolution structured the brain to respond to certain types of experience.26

  Whether caregivers’ c
ompetence would influence the children’s outcomes had not initially been included in the study, but it became a variable to be investigated. This one factor, BEIP researcher Anna Smyke found, made “significant contributions to children’s competence, over and above any other factors.”27

  The BEIP studies officially ended when all of the children had reached 54 months. However, with Romania’s cooperation and MacArthur funding, Nelson and his colleagues extended their study. Over eight years, Nelson and his group found that children who remained in institutional care suffered progressive IQ declines. These results echo Harold Skeels’s and Eva Fillmore’s 1937 report of the IQ scores of siblings surrendered to Davenport by Iowa families. They found that older children’s IQ scores were consistently lower than their younger siblings’, probably because of longer exposure to adverse home environments.28 In addition, in his 1939 report about the Woodward and Glenwood children, Skeels found radical declines in once normal children the longer they lived in Davenport, many to the level then called “retarded.” Skeels’s investigations may be the earliest longitudinal reports of such declines in institutionalized children’s IQ scores.29

  Finally, the BEIP scientists asked a question no other researchers had examined: did institutional and foster care environments literally “get under the skin” and change the children’s brains? To find out, the children’s brain activity was measured using noninvasive EEG readings of three types of brain wave oscillations, called alpha, beta, and theta. Roughly, alpha activity responds to attention, beta to complex cognition, and theta, a slower rate, marks the performance of automatic tasks.30 When tested before the study, the institutionalized children had greater low-frequency theta activity—“as if” Nelson said, “someone had turned down the dimmer switch on the higher frequency . . . [alpha and beta] activity.” By the time the children were age 8, the brain activity levels in those moved to foster care before age 2 was identical to that of children who had never been institutionalized. The study noted that this “catch up . . . required years of exposure to foster care to emerge.”31

  When the children reached age 9, the investigators used MRI scans to study randomly selected subjects from each group. They found that the head circumferences of the institutionalized children were smaller than those in the other two groups, and the MRIs helped explain why. Brain activity takes place within both gray matter—neurons—and white matter—the waxy myelin that coats neurons, allowing quicker connections between areas of the brain. On their MRI scans, children who had been institutionalized showed less gray matter and less white matter: starved of stimulation and affective encounters, their young brains had developed both fewer neurons and fewer connections between them.32 Neuroscience explorations at this level were unavailable when the Iowa group was issuing its reports on the malleability of children’s IQs. In Iowa, intellectually challenged children recovered intelligence when cared for by institutionalized women who made them the centers of their lives. The Romanian orphans recovered when nurtured by caring foster parents who provided stimulation, support, and emotional warmth. Clearly, the message that gets under the skin to change young brains goes through the heart. But how, physiologically, does a reciprocal caring relationship give rise to dramatic brain transformations?

  Nelson and his colleagues’ theories about early brain development drew on neuroscience research from the 1980s, an era when brain studies of early development began to accelerate. Scientists found that infant brains are hardwired to respond to certain stimuli: for example, babies learn the sound of their mothers’ or caretakers’ voices and respond when they hear them; infants perceive patterned light and respond by looking more closely; they learn that crying usually brings food that eases discomfort. Thus, the infant—once thought incapable of meaningful behavior—actively learns to utilize ordinary experience to ensure it is cared for.

  As early as 1962, Yale pediatricians Sally Provance and Rose C. Lipton had studied the behavior of institutionalized infants who did not receive responsive care. They found that by age 3 months, the infants had “tenuous emotional ties” and failed “to establish a personal attachment” to their caregivers. By 7 months, they did not “seek out the adult either for pleasure or when in distress.”33 Their findings (which came from observing infants in an existing situation, not a controlled study) were echoed by BEIP psychologist Nathan A. Fox, who reported the eerie silence of a Romanian orphanage ward in which the babies, in their way “scholars” capable of assessing the response potential of their caregivers, had learned it would be pointless to seek their comfort.34

  With their universal language of babbling, cooing, crying, and reaching their arms and legs into the air, infants “invite” their caregivers into a conversation and “expect” a response. Infants’ inborn developmental program drives that behavior—it helps the baby stay alive—but it achieves far more. This reciprocal communication between child and caregiver, defined by Harvard’s Center on the Developing Child as “serve and return,” is recognized today by neuroscientists as critical for healthy brain development.35 Serve and return interactions open a conversation that literally builds strong connections between brain areas. In the BEIP, the MRIs of Romanian orphans suggested that being deprived of serve and return relationships might impede the growth of brain cells and neural tissue. When the Iowa psychologists told of the absence of interactions between the Davenport children and their caretakers, they were describing just such deprivation.

  Even when caregivers are accessible and well-intentioned, other adverse conditions can harm children’s brain development; for example, poverty, violence, emotional neglect, or abuse each have the potential to increase stress. Like adults, babies and children will never be totally free of all stressors. But in a safe environment, most recover quickly from their alarm at a clap of thunder or the stick of a needle, and as safety returns, they may gain resilience from the experience. However, longer-term adversity, repeated exposure to violence, or the harsh, neglectful environments familiar to the orphans of Iowa and Romania can result in persistent stress that travels a more ominous course.

  A convergence of science findings indicates that such “toxic stress” may harm the developing brain’s sensitive architecture, especially when a caring figure is not available to help the young child manage difficult experiences.36 In chronically high-stress situations, the child’s heart continues to beat faster, blood pressure remains elevated, and stress hormones remain in the circulatory system. Bruce McEwen, of Rockefeller University, a pioneer in the study of the effects of stress on the brain, wrote, “The brain is the central organ of stress because it perceives what is threatening and determines a . . . response that may include fighting, fleeing, vigilance, and anxiety.”37 So it is not surprising that research shows disturbing events may impair not only a young child’s brain development but also their physical and mental health, an effect that may last even into adulthood.38

  In the 1960s, in his lab next door to his Rockefeller mentor, Alfred Mirsky, McEwen discovered the mechanisms for how stress influences the brain. It had been Mirsky who, in 1965, suggested to Skeels and Skodak how environment might have changed the brains of the Davenport children. McEwen, who died in 2020, had remembered Mirsky discussing Skeels’s research and was among the first to show that prolonged stress may impair three critical brain areas: the center for memory, called the hippocampus; the amygdala, which is sensitive to early life stress and regulates mood and anxiety; and the prefrontal cortex, associated with executive function, judgment, and reactivity to social threat. McEwen noted that in a test of cognitive attention, a part of the prefrontal cortex associated with stress showed elevated blood pressure. McEwen and colleague Andrea Danese reported that stress creates “structural and functional abnormalities” in the prefrontal area that especially affect maltreated children and adults and may be related to hyperactivity, substance abuse, and conduct problems, among others.39

  Poverty, and the environmental ills that may accompany it, is one of t
he most pervasive sources of children’s stress. New York University cognitive psychologist Clancy Blair and developmental psychologist Cybele Raver found that poverty’s adversities affect brain development even in infancy. In a 2016 longitudinal study of newborn infants to age 4, they reported that children in low-income environments had smaller gray matter brain volumes—half a standard deviation smaller—than children who had not lived in poverty.40 Another major study compared children raised in poverty (family incomes were under $5,000 per year) with ones in well-off families (with incomes of $100,000–$150,000 per year). The authors found “atypical gray matter development associated with lower social economic status, limited environmental stimulation, and inadequate nutrition of the kind considered critical for learning.”41 And a study in Chicago found that children who had direct exposure to gun violence suffered immediate declines in their vocabulary and reading scores; some recovered from single episodes, but those exposed to repeated gun violence showed longer-term effects.42

  The interaction of childhood adversity with later illness and impaired cognition first came to light with the 1998 publication of investigations of physicians Vincent Felitti, of the Kaiser Permanente health maintenance organization in San Diego, and Robert F. Anda, of the Center for Disease Control in Atlanta. After following over 17,000 mostly white, mostly middle-class subjects for seventeen years, they found a direct relationship between childhood abuse and adult disease,43 including, in 2006, neurological impairment.44 To learn about their subjects’ backgrounds, they developed the Adverse Childhood Experience (ACE) questionnaire—an easy-to-apply tool now used worldwide to assess a patient’s health vulnerabilities related to early adversity. They showed that adults who had endured significant stress as children had measurably higher rates of mental and physical illness and higher long-term risks than those who had not. As Paul Tough, a journalist and author whose life’s work focuses on children’s and teenagers’ educational experience, has noted, “Children don’t experience parental divorce or mental illness or neglect on a specific day; they experience them every day. What the ACE study was really tracing . . . was the influence of adverse environments.”45