(air whooshing) (computer mouse clicking) (gentle music) - [Narrator] We are the paradoxical ape. Bipedal, naked, large-brained, long the master of fire,
tools, and language, but still trying to understand ourselves. Aware that death is inevitable. Yet, filled with optimism. We grow up slowly. We hand down knowledge. We empathize and deceive. We shape the future from our shared understanding of the past. CARTA brings together experts
from diverse disciplines to exchange insights on who
we are and how we got here. An exploration made
possible by the generosity of humans like you. (energetic music) - So I'm now about to
give you an hour-long talk in 18 minutes. (audience laughs) So fasten your seat belts. So here's an outline of what
I'm going to be doing today. I'm going to begin by
providing sort of a conceptual framework for how we think
of the role of experience in brain and behavioral development. Talk a little bit of
the history of what led Romania to abandon and
orphan so many children. Why neglect is bad for the brain. And then findings from this project that Faraneh just mentioned. I'm gonna focus today
disproportionately on behavior and tomorrow I'll turn my
attention to brain and biology. So we need to begin with premise
that experience is really the engine that drives much of
postnatal brain development. That some experiences are,
or at least should be, universal to all members of the species. So for example, sensory
input and caregiving, and these help ensure survival. Others may optimize development. So for example, it's one
thing to have a caregiver who just simply feeds you. It's another to have a
caregiver who is responsive to your needs and sensitive to your needs. Exposure to complex but
age-appropriate language. Age-appropriate cognitive stimulation. In many cases, both classes
of experience have to occur during a narrow window of
time which we often refer to as either as a sensitive
period or a critical period for development to proceed along a typical healthy
developmental trajectory. Two additional points about
experience, of course, if that it cuts both ways. This is a phrase that I
for years I attributed to Bill Greenough and then
Bill Greenough told me actually it was J. McVicker
Hunt who talked about this. So that if a child is exposed
to adverse experiences during this critical
period of development, infection, maltreatment,
lack of caregiving, or deprived of expectable
experiences like nutrition or caregiving, then brain
development can be undermined. And the second is that brain
plasticity changes with age. In some domains, change is
possible throughout the lifespan. For example, barring
pathology, we'll all be capable of learning and memory
throughout our lifespans. But on the other hand,
there are other domains where change is limited
to the first years, for example, vision and hearing. We don't learn to see
better or to hear better. So in today's talk what
I'm going to focus on is what happens to the brain when
there's a profound violation of the expectable environment
during a critical period of development, specifically,
what happens to children who experience profound
deprivation early in life? And then the second question
is can these deleterious effects of early deprivation
be reversed, and if so, are there temporal
constraints on doing so? So, just by way of background,
we know that neglect is the most common form
of child maltreatment in the United States, that
was, I was just trying to impress you with my
PowerPoint skills... (audience laughs) That 75% of all cases of
maltreatment involve neglect. That a particularly extreme
form of neglect is being raised in conditions of profound
psychosocial deprivation such as the 8 million
children around the world who live in institutions. And I should also add that
there are about 140 million orphans around the world. So through the gracious funding
of the MacArthur Foundation, in the late 1990s I was
chairing a research network on early experience on brain development, and two members of the group,
Charlie Zeanah and Nathan Fox and I launched what is now
known as the Bucharest Early Intervention Project which
continues to this day. And there were three goals. One was to examine the effects
of institutionalization on brain and behavioral development. A second is determine if these
effects can be remediated through an intervention, in our case, very high-quality foster care. And the third was to improve
the welfare of children in Romania by establishing
foster care as an alternative to institutional care. In Romania at the time, they
viewed institutional care are the intervention
for child abandonment. So just by way of background,
this really was an experiment in social engineering
engineered by Nicolae Ceausescu, who is this individual here. So in 1966, Ceausescu,
who took over the country, he was a shoe cobbler by trade, had an idea that he
could increase his power if he increased the population. And to increase the
population he set into motion a series of decrees which began
with the menstrual police. So these were state gynecologists who conducted monthly checks
of women of childbearing age who had had fewer than five kids, to make sure they weren't
using birth control or hadn't terminated a pregnancy. He established a celibacy
tax, whereby families received a stipend if they had more than two kids, but they were taxed heavily
if they have fewer than five. And finally, he had outlawed
all contraception and abortion. And the results was that in, before I go to that, was that by the time he
was overthrown in 1989 there were more than
170,000 children living in state-run institutions. So I now want to she
you a brief video clip of an individual now in his
30s who was the byproduct of one of these early orphaned children. (gentle music) (children crying) - So in 1989, communism
fell and the world went to Romania to cover the fall of Ceausescu. There were some medias that
actually found institutions. Institutions that were
never mean to be discovered by the public or the outside world. They left the world in shock that such conditions even existed. - [Woman] Those of us who
visited these institutions built by the communist regime are
unlikely to ever to forget them. Hundreds of children not so
much cared for as contained. - Well, at the age of six months old, I became ill and my parents
tool me to a hospital to be treated for my illness. But instead of finding
healing at a hospital, I actually ended up being
infected with polio. My parents took me a different hospital in Sighetu Marmatiei. They never came back. So the state put me in an institution for handicapped children,
an orphanage known as Home Hospital for the
Irrecoverable Children. - [Woman] What's in this room
no one could prepare for. Filthy, dark, and stinking,
as excrement everywhere. These boys are the most difficult cases. They deserve the best of care,
instead they get the worst. - From the moment that we
could remember for ourselves. That's all we knew. We didn't have compassion, we didn't have feelings or emotions. We just existed to just
vegetate, you know. We were just wild animals
that needed to be caged up, is what we were considered pretty much. - Okay, I think we've see enough of that. So as someone who in my other life studies neurodevelopmental disorders, I actually recognize this phenotype. The difference is that
the disorders I study usually are single gene mutations, whereas these are a
byproduct of the environment for the most part. So we've know for decades
that children reared in institutions are at
very risk for a variety of cognitive, social,
and behavioral problems including disturbances
in social relatedness and attachment, externalizing
behavior problems, inattention/hyperactivity, deficits in IQ and executive functions, and
a syndrome that mimics autism, and then growth stunting. So here's an example of growth stunting. So I want you to be thinking
if these are boys or girls and how old they are. So this is a 17-year-old girl and this is a 14-year-old girl. And as a rule, children lose about a month
of linear growth for every one month they spend in a
highly deprived environment. So the study we did is actually
a randomized control trial of foster care as an alternative
to institutional care. And the way we did this
is that we screened more than 180 infants and
babies, basically kids under about a year or two, to
make sure they didn't have a frank neurological or genetic syndrome. We could only do behavioral exams, we couldn't do blood work and the like. And of more than 180, we wound up with 136 that we considered to
be typically developing. Not easy to do when
you're looking at babies who are nine, 10, or 11 months of age, but they looked to be
typically developing. And also recruited a sample of 72 children in the community that had
never been in an institution, they lived with their family. After an extensive baseline assessment, these 136 children were randomly assigned to either remain in institutional care, what we'll call care as usual, or to be randomly assigned
to a high-quality foster care program that we built, maintained,
and paid for ourselves. The original goal was
to see these children for the first few years of life. So in fact we saw them at
nine, 18, 30, and 42 months, and at 54 months at which
point the intervention formally ended and was
turned over to authorities. And then we thought we would
go a little bit longer, so I found funding at age
eight and we saw them then. And then I was tired of
commuting to Romania, but then I found funding at age 12, and I said, "That's enough." But then we found more money
and then we saw them at age 16. And we were just re-funded
to see them again at 21. In fact, I'm there in
three weeks to launch the 21-year follow-up of these kids. So the three of us who do
this work come from different backgrounds and we're all thick-headed, so when it came time to assess what was the most
important thing to study, this is the short list of what we came up. (audience laughs) Because we really couldn't agree on what were the most
important things to study. I thought naturally it was the brain and Charlie Zeanah thought
it was mental health. So I'm going to summarize just a small set of the findings because of time limits. And all the findings
I'll talk about today, and for those of you here tomorrow, are based on what's called
an intent-to-treat design. There are a lot of ethics involved in this study that I'm
not gonna talk about, but what this comes down to
is that we fully expected over time the children in one group or the other would
change group assignments. A classic example would be a child who is randomly assigned
to the institutional group, the authorities decided that
child should be reunited with their biological family,
or that child should go into government foster care or be adopted. We had no say in this. We didn't interfere in this. But over time, children
changed their group assignment. But, we analyzed their data based on their original randomization schedule because that avoids the
pitfalls of sample bias. So I'll start with IQ
and then move from there. At baseline, when the kids on
average were about 20 months, using the Bayley exam, you
can see that the children in the institutional group are actually below the cut point for
intellectual disability compared to the children in the
never-institutional group. So then the question is what happens following random
assignment to foster care? We'll start with this. This is going out to 54 months. At every age, you'll see that
the children in foster care have markedly higher IQs than the children in the institutional group. And here the more
important finding is that, this is only foster care. The children placed under
the age of two have markedly higher IQs than the
children placed after two. Even as late as 12 years of age, what we see is we still
see an intervention affect. Here's full-scale IQ,
never-institutional group, foster care group, institutional group. And one thing to keep in mind
is that this intervention was not designed as a
cognitive stimulation program. It was designed to build relationships. So we didn't have any idea that
IQ would benefit like this, but nevertheless, we continue to see this
and we see no washout. Even through 16, where we're
now going through the data, we still see an intervention effect. So young children living in institutions show reductions in IQs. Removal from institutional
care and placement into high-quality foster care
before two leads to a recovery, although not full recovery. And we see stability across
the first 12 years of life. The one thing I'm not
going to show you is that when we look at placement disruptions, because it turns out
because of the authorities, there were kids who made
multiple placements. They went from the institution back to their biological family, re-abandoned, then to foster case. The children who show
more placement disruptions have much less favorable outcomes. Stability matters. Turning now to attachment,
the question now is if you look back 50
years in this literature, what you often see are disturbances in attachment behavior. So this is the relationship
a child has with a caregiver. And so we assume that these
perturbations in attachments early in life could alter the trajectories of other aspects of
social-emotional development. So let me give you an example of this. This is what's called
the strange situation. This is a manipulation
where a child is in a room with a caregiver and maybe some toys, and then a stranger walks in the room. You see how the child
behaves with a stranger. Then the caregiver leaves, you see how the child
interacts with stranger. The the stranger leaves and is left alone. And then an adult comes back in the room and you see how they respond. So this is an 18-month-old and I want you to watch what goes on. So right now this is the phase where the child's been
left alone with the toys. (woman speaking tenderly
in foreign language) So this looks like a
classic reunion episode. He jumps into her arms, holds onto her. But that's the first time
he's ever met this woman. And that's sort of the
indiscriminate behavior that is very common among kids
with histories of neglect. In fact, Mike Rutter, the
distinguished child psychiatrist in the UK, argues that
this part of a syndrome, of institutionalization syndrome. So what we see at baseline is among the
never-institutionalized children, about 70% look like they
have a secure attachment. The same number of
institutionalized children have an insecure attachment, so it's profoundly disruptive at baseline. Now if you look at the intervention, the children placed in
foster care before 22 months, 70% have a secure attachment. The children placed in
foster care after 22 months, 70% have insecure attachment. So we see that same
inflection point at 54 months and then again at eight, and
the findings are the same. We did a functional measure
of attachment behavior. And what we did is that we
arranged with the caregiver or the mother that we said, "Someone was gonna knock on the door. "Let your child answer the door "and let your child do
whatever they want to do." So with that arrangement, the
stranger knocked on the door. The child answered the
door and the stranger said, "Come with me, I have
something to show you." It took a lot to get this
through our ethics board. And this is sort of every
parent's nightmare, right? And the question is will
they walk out the door and walk off with a complete stranger? If you look at the institutional group, more than 50% of the kids
in the institutional group walked off with a complete stranger. That was cut in half for
the kids in foster care. And there was one in the
community who did that so we've been monitoring
that child for 20 years now to see why they did that. So children experiencing
early institutional care are far more likely to develop
disturbances in attachment than those who did not. Children randomly assigned to foster care following institutional care, particularly if they were
younger than 22 to 24 months, are more likely to show an improvement in attachment behavior. Lastly, what about the brain? So we assumed the behavioral phenotype that we'd been observing all
these years has its origin in alterations in brain development. And so we've done lots
of different things. Over the years we've done EEG and now we've been doing MRI
for the last decade or so. I'm only going to talk about the EEG data. So the way to view this
is we place censors on, well you can see that in this child here. We place censors on the child's head and we can record the
brain's electrical activity. We can color code it, so red would reflect more activity, green would reflect less activity. And what you're looking at here
is a view from the top down. Here's the nose, back of the
head, left ear, right ear. And notice how much more brain activity there is in the
never-institutionalized group compared to the institutionalized group. If you move to the foster care placement, this is at age eight. Institutionalized group, foster care after two years
of age, and they're identical. Foster care before two years of age, never-institutionalized
group, they're identical. So the same inflection point that we see in IQ and attachment, where there's a cut point some
time around 20 to 24 months. So children who received the care as usual displayed deficits in the
brain's electrical activity compared to kids
randomized to foster care. Children who received the
foster care intervention continued to show typical
levels of brain activity through age 16, not just eight. And age of placement into
foster care was associated with an increase of alpha power. So there are a lot of changes in Romania. Basically because of, in part this study, they changed the law
that children under two could not be institutionalized
and under three. And if you look at the
statistics of the number of kids living in
institutions, it's plummeted. So the bottom line is let's
learn from the science. Let's inform policy makers,
politicians, and clinicians about the short- and long-term
effects of early neglect, but in particular that
the duration of time spent in a neglectful environment powerfully influences later development. I really can't talk any faster than this. (audience laughs) Age of a child when removed
from a neglected environment and placed into a family is also critical in influencing the outcome. Early neglect can have life-long effects on both psychological
and physical development. And finally, these
findings are not limited to children growing up in institutions, but rather generalized to
any child experiencing early and profound deprivation such
as parent-child separations. Thank you. (audience applauds) - I'm going to be talking
about what it's like for children who have
suffered early damage to their hippocampi, the
memory structures of the brain, to grow up without episodic memory. So just to give you an idea of what episodic memory is all about, it appears to be an
exquisite cognitive system which has recently
evolved in modern humans. It's a late developing
function and, unfortunately, it's an early declining
one as well, in old age. It's oriented toward past
memories that we have accumulated over a lifetime and it's
vulnerable to neurological injury. Incredibly, it enables
us to mental time travel to the past and also
to plan for the future. It allows us conscious re-experience of personal autobiography and
maybe, it's unique to humans. This constellation of incredible abilities that we humans possess is
dependent on a brain structure called the hippocampus, which you can see on the right-hand side
of the slide in blue. And episodic memory is dependent on the integrity of this structure. You see also the amygdala shown in orange behind the head of the
hippocampus called the uncus. And the amygdala is the center for regulation of our emotions. Hippocampus appears to be
critical for our memories. So what are the risks to the
integrity of the hippocampus, particularly during early development? Oxygen deprivation seems to
be one of the critical factors that can expose babies when
they come into the world, for a variety of reasons, to
early hippocampal pathology. One type of risk is
children who have congenital heart defects and they
require open heart surgery during the first days of
life because of various anomalies of the heart
that need to be set right. Extreme prematurity
seems to be another kind of risk factor because of
the lung insufficiency. And also babies who have to
be put on heart-lung machine in order to give time to
the clinicians to treat them appears to be yet another risk factor. Whatever the etiology is,
exposure to lack of oxygen appears to start a chain of reactions
which is in a causal sequence. It starts from oxygen
deprivation leading specifically to damage of the hippocampal structures, and then in turn, leading to the emergence of a memory problem later in childhood, which can range from moderate
to developmental amnesia which I will be describing in a minute. So I wanted to give you a
feeling for the trajectory of cognitive development
after such injury occurs. Parents are usually extremely
happy because their children have passed this critical
stage of being seriously ill. And they think that everything
is over because physically the children actually
make a very good recovery. So from birth to two years,
they develop normally and they acquire all their
developmental milestone as expected. Between the ages of two to three years, they develop good speech
and language abilities. They go to nursery
school, they learn songs, they learn rhymes, their
motor development is normal. And really don't parents don't suspect that anything is wrong at all. Then around three or four years of age, they start preschool programs
and there they excel as well. They develop sight reading,
they do copying and drawing, and they do all kinds of
normal developmental milestones and they achieve as normal children would. However, around the age
of four to eight years, they start showing the first
signs of an amnestic syndrome. They forget their belongings, they start repeating questions,
they forget instructions, they forget messages, they
tend to get lost in new places, they appear to be confused, and they are unable to
remember their lessons. This is very strong evidence
that they're growing into a deficit which only becomes
apparent with increasing age. And this is the way that
typically the way the children present to my clinic when they come, because the parents don't understand where this problem actually came from. So the parent usually says, "My child seems to be
living at the moment, "doesn't seem to be bothered
by the past or the future, "and cannot plan for anything." The child seems to have a flat affect, and that's important to note. They're not demanding children, they're very easy to live with. And for those of us who have children, we know what it's like when
a child wants something. They won't let go of the
idea until they get it. Well these children are not like that. They forget what they want. They're also very disorganized. The teacher says that they're
very friendly and polite but they're too laid back. And they seem very able, but
when it comes to the crunch, they can't deliver. And the patient says, "I listened
in class and I understood "everything that was
said, but a little later, "I couldn't remember anything." So you have to realize that there is no neurological symptoms. This is a silent damage
that shows its symptoms and there's no evidence of any kind
of neurological abnormality. So we start assessing these children. The first, neuropsychologically, find out what the problems are. And we discover that
there's a set of weaknesses that they all have and
there's a set of strengths. The set of weaknesses are
defined by inability to be able to remember the events of their life. They are unable to recall and
they also do not recollect. Recollect is a very subjective experience, but they don't seem to even understand the concept of recollection. On the other hand, they have strengths. They have fantastic factual memory. They are like a dictionary of knowledge, but without context. They have very good recognition. So if they have seen
something and you show it in a multiple choice fashion to them, they know which one it is
that they have seen before. And they have a sense of familiarity. The neural substrate of
their weaknesses appears to be a very marked, but fairly selective, bilateral hippocampal atrophy. On the other hand, the
set of strength seems to be the integrity of
the parahippocampal cortex which appears to be relatively preserved. So our first task after
having neuropsychologically assessed these children and
shown these disassociations, there are three of them,
three disassociations. Our next was to actually verify
that there really was damage to the hippocampus because
all these weaknesses that I have described
are actually dependent on the integrity of the hippocampus. So we needed to be able to demonstrate that the hippocampus is in fact damaged. What you see here is zero
is set at the volumes of a large group of normal controls. And then in black you see the volumes of the hippocampi in the normal controls. Then you see the volumes
of the orange cases. These are cases with moderate
degree of hippocampal pathology ranging from
15% to 25% of normal. And then you move to the left-hand side where you see the red bars. The red bars are individual cases of amnesic patients that we have seen. And as you can see,
reductions about 30% to 75% actually counts as
severe enough to warrant the kind of amnesic syndrome
that I have described. So you can see the significant difference between the three groups there. The moderates and the
controls are not significantly different from each other,
but the amnesic patients are. Below that you see the
volumes of the amygdala. Unlike the volumes of the hippocampus, the volumes of the
amygdala are not reduced. Here you see the work of Loic Chareyron, who has been measuring the volumes of the hippocampal subfields. Although the entire hippocampus is reduced in volume bilaterally, the
magnitude of the impairment or magnitude of the reduction
is far more pronounced towards the posterior
part of the hippocampus. In fact, the head of the
hippocampus, the uncus, is relatively spared. And then you see the
other subfields are also significantly reduced in volume. So what does this do to a
child who comes into the world seemingly normal, because
they've recovered from the injury that they've had, apparently. But they do develop normally in many ways, except in this memory domain
that I have just mentioned. Here you see the cognitive
profile of patients which developmental amnesia
during early childhood and later on as adults. So there're 18 of them
that have been studied and they're matched with 18 controls. The age range is from 11 to 35. And the most remarkable thing here is the mean memory quotient
of this group is 61, which is in the
significantly impaired range, compared to their mean memory quotient of the normal controls which is 108. These are standard scores. On the right-hand side, you see the performance of
the amnesic group relative to the control group on these measures: on full-scale IQ, working
memory, literacy, and numeracy. So immediately it's obvious
that these children have developed these skills without
the aid of the hippocampus. So these skills are not dependent on the integrity of the hippocampus. So what do they have problems with? Well, they have problems
with episodic memory. And that is captured in this
test which actually asks for them to remember a
name, a belonging, a route, a simple route, recalling
a story, an appointment, pictures of faces, messages, et cetera. But when you look at their
ability to be able to associate semantic items together
or to remember vocabulary, they do extremely well as normal. So this is the first
disassociation that we are able to see very easily in these patients. The second disassociation
is an inability to be able to recall, but a very good
ability to be able to recognize. This is tested a through a
paradigm that has been developed by Alan Baddeley and his colleagues, where he presents for recall verbal items such as remembering a name and
a profession of individuals, four individuals actually,
repeatedly presented for recall. And in the nonverbal domain,
they're asked to copy shapes. Simple shapes as you can see
there for nonverbal recall over three trials, and then
they have to recall them. For recognition, they're
given a very difficult test of verbal recognition
where a list of 24 words of names of individuals
is presented to them. And then later on, they're given multiple choice
for each of these items. That's for verbal recognition. And for nonverbal recognition, they're shown a list of 24 doors. And then later on they're
given four alternative choices of very similar doors
and they have to identify which one they had seen before. So if we look at the performance
of the amnesic patients relative to controls, we
see that for recognition, both verbal and nonverbal,
they're actually doing very well compared to the controls. But there's this proportionately
reduced performance when it comes to recall
where they cannot recall the names and the professions
of those individuals that they had seen, nor
able to recall the shapes that they had learned. And this ability to
recognize is not correlated with the volume of the hippocampus, as you can see on the
right-hand side of the screen. But it is correlated
significantly with the volume of the hippocampus for both verbal
recall and nonverbal recall. So this is the second disassociation. Now we move to the third disassociation which is actually very
difficult to demonstrate. The reason is that recollection
is a subjective experience. And if we ask the patients
to recollect something, they don't even understand
what the terms means because they've never been able to do it. They don't even understand what recollection experience is like. But it is bringing mind to something that they have experienced before. So Emrah Duzel, in
collaboration with our group, tried to get a neurophysiological
record of recollection. This is an EEG experiment and
evoked response experiment whereby the patients were
presented with a list of words, about 80 of them, and they
had to judge each word and say whether they found it
to be pleasant or unpleasant. And then later on a test. They were given another
list of 80 words mixed in with the words that they had seen before and they had to judge
whether it was a word that had been seen before or not. So it's a recognition paradigm
which they should be good at, but they have to recollect, and at the time the EEG is being recorded. So what you can see on the
left-hand side of the screen is that in the early time window, we get this modulation which
is called the N400 modulation. And this modulation is associated with the feeling of familiarity,
something appears familiar. It doesn't involve recollection. But later time window,
around 600 milliseconds, you get this second modulation which is called the
late positive component. This late positive component
is supposed to reflect the generators of the hippocampus which gives you a feeling
of recollection so that you can remember whether you
found it pleasant or not. And as you can see in the normal controls, you see these two modulations, both the early one and the late one. But when it comes to the patient
with developmental amnesia, you get the early modulation, but the late positive
component is missing. Similarly, when you look
at the topographic scalp distribution of early versus
late evoked responses, you see that the N400 effect
is present in the controls, but it's also present in the DA patients. But the late positive component, which is a reflection of recollection, is present in the controls but it's blue and absent in the DA patient. So this is a measure
that of course, as I say, is a measure of a subjective experience. And a subjective experience
is very difficult to capture by behavior. So we next turn to an fMRI experiment which is even more complicated, but I'll try and simplify it for you. It's using a paradigm
of paired associates. Paired associates is a paradigm that really requires the
hippocampus' engagement. So patients are shown, patients
and controls, are shown a word paired with a
scene and they have to try and remember the pairing of
the word with that scene. And some of the scenes are urban scenes and some of them are rural scenes. So they see a huge number of
these words paired with scenes. And then afterwards,
they go into the scanner. And you can see that their
performance is actually very poor compared to controls who are
significantly above chance. They get chance-level performance. But when we unexpectedly,
we did not expect this, but when you actually look at
the activation in the brain we see that the activation is very similar to that of the normal. In the normal controls, you see activation in the
parahippocampal cortex and in the retrosplenial cortex, which is the network
of scene reinstatement. And in the patients you get almost exactly the same pattern of activation. However, their brain remembers but they cannot remember
the performance themselves, as indicated through the button pressing that they have to do. So I'll quickly go to the next one. To summarize, so what
are the memory processes in developmental amnesia then? We know that they can encode. We know that they can consolidate. We know that they can retrieve but only through
recognition and familiarity, not through the
hippocampal-dependent processes of recall and recollection. This then gives them the
so-called deprivation that they cannot really subjectively experience their autobiography. So what is autonoetic consciousness? It's the human ability to
mentally traverse across time and be able to examine one's own thoughts, and the sense of self
that affects our behavior in the present, past, and future. Best captured by this passage
from Teilhard de Chardin where he says, "In the passage of time, "a state of collective human consciousness "has been progressively
evolved which is inherited "by each succeeding generation
of conscious individuals "and to which each
generation adds something." That seems to be the type of experience that patients with developmental
amnesia do not possess. But I don't want to leave this giving you the impression
that it's all negative. In fact, it's very uplifting
because I was having a conversation with one of our
patients and I was asking him if whether his memory
was a problem for him. And he said, "No, my memory
is not a problem for me, "it's a problem for you." (audience laughs) So I said, "Well, how come? "Don't your friends get upset with you "because you can't
remember your appointments, "you don't do the things that
you've promised them to do?" He says, "No, on the contrary. "My friends are very happy with me." I said, "How come?" He says, "Well, for one thing,
I don't carry a grudge." (audience laughs) So I thought, really,
our memories are a gift and we have to use it
for the power of good. Thank you very much for your attention. (audience applauds) - As you've heard, we live in a time where
there's growing concern, not only about the potential
life-long impact of deprivation and early adversity in childhood, but we also live in a time of
global adversity with rapidly increasing natural disasters,
rising political conflict. We have the largest number
of refugees, we think, we've ever had in human history right now. And we're just at the beginning stages of what's going to happen
with climate change. And yet, my theme here today
is despite these disturbing adversities, and their increase, there's evidence of
resilience all around us. And we'd better figure out
how to mobilize that capacity to address the scale of problems we have. And many of the issues we've
heard about today and many of the global mass trauma
threats to human existence in the world today are
multi-systemic in nature. And for that reason, this is my preferred
definition of resilience. Resilience is the capacity of a system, could be a child, could
be family, an economy, a lake, a global climate, a society, but the capacity of a
complex adaptive system to adapt successfully to these challenges that threaten system function,
survival, or development. And the reason I think it's important to have this kind of a
definition is because if we're going to deal with
the complexity of the threats facing child development
and life on the planet, we have to be able to integrate
our sciences across levels. We need a definition a
definition of resilience that is scalable from a molecular
level up through various increasing macro-system
levels of social organization. And we need a way to
integrate what we know about ecological threats with what we know about social and other kinds of threats. And I also think we need a definition from a developmental
perspective that is consistent and recognizes that human
beings are developing systems. And I particularly do a lot of research with living systems like
this child and the families in which children are nurtured. But development emerges from
many systems interacting over multiple levels. It's an emergent phenomenon. And we also know that the
systems of a child's life are not only interacting all the time, but they're embedded with
each other and interconnected in such a way that a child's
experience is influenced both directly by some of the
systems they interact with. Their family, their friends, they go to school eventually
and interact with schools. But also by the systems
indirectly connected to children. There are national policies, they're community resources
that indirectly affect the development and
well-being of children. And my picture here is just
the socio-ecological systems. Of course, there's
systems within the child that you've been hearing about all day and those can be incorporated
into the picture as well. So from a systems perspective,
resilience is dynamic. It's changing over time because human beings
are changing over time. They're developing, they're constantly interacting
with other systems. And the capacity for
adaptation that you or I have, or any child, is
distributed across systems. It isn't just in the child or
just in the individual person. Because you can draw on capacity
and resources that you have access to via relationships
that you have with people, like social support and many
other systems that can provide you with help and support
of many different kinds. Also, child resilience doesn't just depend on many systems outside the child. It also depends on the
resilience of those systems. This is strikingly apparent
in a major disaster when all the systems collapse at once. And then we all realize
how dependent we are on the operation of many other systems to function in the world. This kind of model also would suggest there's going to be diverse
pathways of adaptation. There's not just one way, one
path that reflects resilience but there's many different
paths of adaptation. Depends on many different individual and contextual differences, as
well as development itself. Now adversity matters. And this is a typical risk gradient here. These data happen to come
from an emergency shelter focused on eight- to
ten-year-old children. And what you see here is
that if you're already in an emergency shelter, but
ignoring that for a minute, if you just count up these
major risk factors that are present in the life of
the individual children here, you can see that the
more risk that's piled up in the life of the children, the more problems they're
exhibiting on this measure. But that's on average. And what those kind of pictures don't show is the variation within risk levels. So we know that, on average,
problems with health and behavior increase with
the piling up of risk factors, but we also see a lot of variation. And the resilience investigators
from the very beginning were fascinated by trying
to understand the people represented by the white spots here. The people that are doing
okay, are doing very well, even though they have been
exposed to a lot of risk factors. How do we account for that? Here's a different kind of risk gradient. This one is longitudinal. These are growth curves. These are based on all the
reading achievement data in the Minneapolis public
schools over a five-year window of time where they
kids were tested every fall, which they routinely do, using
administrative data here. And we've divided the
children into four groups to illustrate a continuum of risk. The solid line there in the middle is your norm reference point. This test is designed for growth, so it's measuring increases over time. And what you're looking
in the solid line is around the 50th percentile
expected growth. The bottom group are kids
who've experienced homelessness at some time during the whole window of this period of the study. And we were surprised to see
that 14% of the students in the Minneapolis public schools
had experienced homelessness. Usually they're picked up when they enter an emergency shelter with their family, but there's other ways. Sometimes people, you know, are doubled up or living on the street
or something like that. But these kids are pulled out first. So they've experienced homelessness. It doesn't really matter
a whole lot when it was. This is an indicator of high risk. And you can see here
their reading achievement in the third grade starts
around the 12th percentile, on average. And their achievement is
significantly lower than kids who qualified for free meals,
who're living in poverty but have not experienced homelessness. And both those groups who
are very disadvantaged are achieving at a much, much lower level than the norm reference point. And then if you look at the top group, those are kids who have
not experienced free meals or homelessness, that's the
only way that they're low risk. But they start off at the 75th percentile on reading achievement and stay there. What you're looking at
here is the extraordinary achievement disparities that
many cities are worried about. And we are particularly
concerned about in Minneapolis, 'cause we have very achievement
overall in our state, but horrible achievement disparities. And this is a huge issue. We're talking about between that top group and the bottom group, a four-year
difference in achievement. It's a huge gap. But that's not the
whole story here, again. If you take the bottom
group and now look at them as individuals, at their
individual growth curves, you see this scatter plot
here, the famous spaghetti plot where you cannot make out any individual. However, all of you'll
just have to believe me when I tell you that we're looking at a five standard deviation range here. What hits you when you see
it this way is the variation. And about 45% of the kids in
this group are doing okay, meaning average or better,
on both reading and math throughout the entire period. And those kids clearly
have a different situation or different resources than
the kids who are achieving at the first percentile along the way. And these kind of data beg the question, what accounts for this? What makes a difference? Because we'd like to know
what make a difference so we can make progress on addressing these kinds of disparities. So there's been a lot of
research on this topic. School district data sets can be great but they don't have as many
of the protective factors of interest to people like me as I'd like. So you have to do some
other kinds of studies. In these data, we do know
that attendance matters. It turns out that homeless kids don't attend school as often. They miss a lot of school and that does affect reading scores. It also turns out that a
one-minute reading test in first grade predicts both the intercept and the growth here in
these growth curves. So where you start off does matter. So there's been decades
of research on resilience. And what's I've highlighted
in this slide is some of the most common protective factors that have been observed in many
different kinds of studies. What's striking is that
despite all the different types of adversities that have been studied, ranging from war experiences
and being a child soldier to divorce or child
maltreatment in the home, that a small number of protective
factors keep turning up in many different kinds of studies. And this led me in this book
and other places to talk, to describe the short list. What I mean by that,
these are the most salient protective factors that
stand out in this literature. And on the right-side I've
listed what I would think would be implicated as
the adaptive systems that account for those things
on the short list. And I would argue that these, we've heard about some of these today, but these are probably the human legacy of both biological and
sociocultural evolution. That's why they're so pervasive
in different situations and cultures around the world. Another interesting thing
I wanted to show you about what we've learned
about resilience is that in the history of the science,
the study of individual child resilience preceded
almost entirely separately, surprisingly enough, from the
study of family resilience at the family system level. The different group of researchers, they hardly ever interacted. And now they're beginning
to put their story together. And what I did in this
article was just take the two literatures and line up
the protective factors that are frequently described. And they show, I think,
very striking parallels across different kinds of factors. And I don't think that's coincidental. I think we're looking at either systems that are constantly interacting so they're part of larger systems, or they've co-evolved. But you can tell me what you think later. There are a lot of roots of
resilience in early childhood. And you know, there's great
summaries on that literature of why early childhood is so important. And this website here, the Encyclopedia on Early
Childhood Development, has a lot of information on that topic, as well as resilience. But what we've learned
is that families matter in multiple ways. And what we've heard a lot
about today underscores decades of evidence that
either the absence or loss of caring parents, or the
presence of harsh neglecting care, especially in early childhood, threatens and can have
life-altering consequences for human development that lasts
throughout a whole lifetime and possibly now even
into the next generation. Adversity in early childhood
around losing the quality of care, or not having it,
creates a kind of double jeopardy for kids in early childhood. Because not only do they
currently lack protection, but the absence of good
quality care undermines the development of many
domains of competence and compromises future
resilience of children. And we know that interventions
that improve parenting, many different kinds of
interventions that focus on boosting up parenting,
whether it's foster parents, natural parents, or adopting parents, promote positive development. It seems to be a very
powerful protective systems. And in some cases, you
get cascading effects, and we need to know more about when we do and when we don't. Here's some data from
research in shelters, where I've done a lot of
research over the years, locally in Minnesota,
showing the moderating effect of parenting quality on child adversity. These are young children,
like four- to six-year-olds, whose families are staying in shelters. Very high risk group. What you can see here, we can use different strategies
of measuring parenting. On the right you have an
outcome of academic functioning, how well the child is functioning in terms of achievement and academic things. And you can see here
there's both a main effect for good parenting quality
and a protective effect. So good parenting always is associated with better academic achievement, but in high-risk situations
it's even more important, so you get an additional effect. On the left you see a graph
for child trauma symptoms. And in this situation, when
adversity is really low, you don't see much in the
way of child trauma symptoms. But as adversity rises, you begin to see these symptoms
and then you also begin to see the moderating
effect of good parenting. And in that particular study, the parenting was measured
by observational coding in structured parent-child interaction. Child skills also matter. And there's a lot of interest right now in executive function skills. And I see a lot of you out there
using your executive skills listening to these talks
and paying attention, figuring out slides and so forth. But children need these kind
of cognitive control skills to even enter kindergarten
and begin to learn. They have to be able to
listen to the teacher, sit on the circle, control
their behavior, and so forth. And there's been a lot of
interest in these skills because they predict school
success and they do it particularly well for
very high-risk children. Here's some data, again from research
with homeless children, where we assess their
executive function skills using a battery while
they were in shelter and then follow them to
kindergarten and first grade. And we find the kids that are doing well, both in terms of learning and behavior, have better executive function skills. And that's led people, our
group as well as other groups, to try to focus on boosting
executive function skills. Those interest loads of
people because they show high plasticity during
the preschool window, so we may be able to boost up the school readiness of children. Education also matters. And schools have a lot
of the same features and characteristics of
healthy effective families. And I won't dwell on that, we can talk about it later if you like. And communities also matter. There's less research on
the ways in which effective communities bolster
resilience in the families and children that live
within those communities, but there's a lot of
interest in that right now to try to understand how that works. And there are important protective
systems at other levels, both within the individual at
the neurobiological levels, and there's also a lot of
interest in the capacity that's embedded in the great religions and many cultural systems around the world. And I didn't have time to do that here, but those also line up
with the short list. So children never could wait on scientists to figure it all out. If you have a child in your
office or refugee camp, you have to act based on what you know. And so as the science developed, people have tried to translate what there is knowledge from
resilience basic science and intervention research into practice. And this, just this general process, has had a transformative
effect on practice and shifted the focus away from just risk and vulnerabilities to
protective processes, and the idea of building
capacity at multiple levels. So I want to close by
saying there's evidence of resilience all around us. That what I think of as
ordinary human adaptive systems, nothing rare and extraordinary about it, but these ordinary adaptive
systems are very powerful. Resilience can be nurtured and promoted. And the resilience in children depends on the resilience of many
interconnected systems, and in particularly on the
supports that are embedded in their proximal systems
of families and communities. We can build resilience in
early childhood programs and it's important that
we focus on that based on what we've heard today and based
on a lot of other evidence. That there's a very high
return on investing in early childhood because there are
multiple cascading effects across levels and across domains. And I'll just close by
showing this picture. I offer a MOOC on Coursera
on the topic of resilience in children from a global perspective, and it's fun to have people join in to the discussion forums on that MOOC. Thank you for your
executive function here. (audience applauds) (gentle music)
