In the previous lectures, I
discussed the various processes
involved in conscious
behavioral actions,
such as language and reading.
It's important to
consider that, in addition
to conscious behavior
such as these, our bodies
and our brains also engage
in unconscious processes,
such as developing emotional
responses to perceived stimuli.
As we will see,
the neural biology
of the emotional response
system has many characteristics
in common with the
conscious response systems,
such as language and reading.
Recall from our
last lecture that we
used the example of how
various parts of the brain
are involved when we develop and
perceive an emotional response
to a stimulus.
Various parts of the
cerebral cortex as well as
parts of the subcortical
areas, such as the hippocampus
and thalamus, communicate with
an area of the brain called
the amygdala, illustrated here.
The function of the amygdala
is to receives sensory stimuli
from other parts of the
brain and decode them
in the form of emotions.
If we feel a certain
type of emotion,
whether anger,
sadness, or pleasure,
that perception probably
came through the amygdala.
As described here,
the amygdala also
plays a central
role in our ability
to sense potential danger in
the surrounding environment
and to mount a response to it.
Sometimes that
danger is in the form
of potential physical harm.
Sometimes it is in
the form of something
that creates a sense
of emotional stress,
without the actual fear of
immediate physical harm.
In either case, our body
has developed a mechanism
to respond to the perceived
danger or stressor,
using a combination of conscious
and unconscious processes.
The body has developed a very
effective unconscious response
to stress that involves both
neurological and hormonal
components.
Once the amygdala has
conveyed to the hypothalamus
the presence of a
perceived threat,
or other type of a
stressor, the hypothalamus
triggers a series
of steps in response
to the perceived stress.
The first of these
is to communicate
with the pituitary gland, using
specific hormonal substances
referred to as
releasing factors.
When the pituitary gland
senses these factors,
it sends a message
to the adrenal gland,
the body's principal
stress response mechanism.
The adrenal gland, which is
located close to the kidney,
rapidly secretes
into the bloodstream
a series of hormones, principle
of which are epinephrine--
commonly known as
adrenaline-- norepinephrine,
and cortisol-- commonly
known as cortisone.
The level of these circulating
hormones in the bloodstream
is referred to, collectively,
as the allostatic load.
While a short-term stress
response of this type
is a protective response
to perceived stress,
chronic exposure
to stress can lead
to a chronically-elevated
allostatic load.
Chronic elevation of
one's allostatic load
can be harmful in
a number of ways
due to harmful effects
of prolonged exposure
to stress-response hormones.
Chronic elevation of
the allostatic hormones
can have harmful effects on
the lining of important blood
vessels.
The first step in this
process is an inflammation
of the cells that make up
the lining of the vessel.
As with any chronic
inflammation,
over time these cells
will start to lay down
scar tissue in the walls
of the blood vessel.
This scarring leads to stiffness
in the wall of the blood
vessel, with corresponding
increase in blood pressure
and reduced circulation to the
organs fed by the blood vessel.
As a consequence
of these changes,
the risk for a range
of chronic diseases
increases, especially
cardiovascular disease
and kidney disease.
Writing in 1999,
McEwen and Seeman
described the potential
health consequences
of chronically-elevated
allostatic load.
They reported,
"Allostatic load appears
to be a useful construct
for conceptualizing
how 'wear and
tear' and increased
morbidity and
mortality are caused
over long-term intervals,
not only by the more
dramatic stressful life events
but also by the many events
of daily life that
elevate activities
of physiologic systems."
They go on to say that,
"Allostatic load reflects
the impact not only of
life experiences but also
of genetic load--
individual habits reflecting
such items as diet, exercise,
and substance abuse,
and developmental
experiences that
set lifelong patterns of
behavior and physiological
reactivity."
These authors bring
up the important point
that chronic elevation
in the allostatic load
can be the result, not only
of inherited genetic traits,
or of stressful experiences, or
unhealthy behaviors as adults,
they also suggest that early
developmental experiences
in infancy and childhood can
have potentially life-long
consequences in this area.
In 2012, the American
Academy of Pediatrics
released a report that
summarized recent research
on the ways early
child adversity can
affect both child health
and subsequent adult health.
Echoing the comments
of McEwen and Seeman,
the committee that
conducted the study reported
that "Longitudinal
studies that document
the long-term
consequences of childhood
adversity indicate that
alteration in a child's ecology
can have measurable effects
on his or her developmental
trajectory, with
lifelong consequences
for educational achievement,
economic productivity, health
status, and longevity."
Jack Shonkoff, the principal
author of the Pediatrics
Technical Report,
made similar comments
in an article published in 2009
in the Journal of the American
Medical Association.
Shonkoff reported that children
from families and communities
with low income and
low educational levels
may be especially vulnerable
to the biological embedding
of disease risk because of
their disproportionate exposure
to highly stressful influences
such as neighborhood violence,
dysfunctional schools, personal
maltreatment, household chaos,
and absent parents."
The American Academy
of Pediatrics Report
suggests that particularly toxic
forms of stress, experienced
over prolonged
periods, can actually
alter the anatomic structure
and pathophysiologic processes
of a young child.
The report states
that, "Toxic stress,
can result from
strong, frequent,
or prolonged activation of the
body's stress response systems
in the absence of the buffering
protection of a supportive,
adult relationship.
Such disruption may
result in anatomic changes
and/or physiologic
dysregulations that
are the precursors of later
impairments in learning
and behavior as
well as the roots
of chronic, stress-related
physical and mental illness."
How are we to
understand the comment
that toxic levels of
stress experienced
by infants and young
children quote,
"May result in
anatomic changes and/or
physiologic
dysregulations that are
the precursors of later
impairments in learning
and behavior as well as
the roots of chronic,
stress-related physical
and mental illness,"
as those authors report?
The human response
to stress involves
both conscious and
unconscious perceptions
of stimuli from the environment.
The conscious
perception of stress
is mediated by the visual and
auditory cortex as well as
the frontal lobe,
with signals conveyed
to the basal ganglia and
the adjacent thalamus
and hypothalamus.
A more rapid,
unconscious response
connects the amygdala,
hypothalamus,
and pituitary gland.
As with the more
conscious activities,
such as language and
reading, these parts
of the brain's unconscious
emotional response system
aren't connected together
by white matter axons.
As with other types
of axonal connections,
the more frequently
these axonal connections
are triggered, the more likely
they will become milonated
and the more rapidly they
will conduct their impulses.
This brings up an
important question.
As a consequence of a more
frequently activated stress
response system,
will a child, raised
in a stressful environment, also
develop an exaggerated response
to stress with chronically
elevated allostatic load?
The pediatric report goes on
to describe the specific ways
that early and prolonged
exposure to toxic stress
can actually alter the structure
and function of a child's
brain.
"Exposure to
stressful experiences
has been shown to alter
the size and neuronal
architecture of the
amygdla, hippocampus,
and prefrontal cortex,
as well as lead
to functional differences in
learning, memory, and aspects
of executive functioning.
Thus, the developing
architecture of the brain
can be impaired in
numerous ways that
create a weak foundation for
later learning, behavior,
and health."
"Hence, altered
brain architecture
in response to toxic
stress in early childhood
could explain, at least in
part, the strong association
between early
adverse experiences
and subsequent problems in
the development of linguistic,
cognitive, and social-emotional
skills, all of which
are inextricably intertwined
in the wiring of the developing
brain."
This concept, that the
anatomical structure of neurons
and their axonal
connections can be affected
by factors in the
external environment,
is referred to as
epigenetic imprinting.
The DNA of the genes a child is
born with it will not change.
However, the manner
in which those genes
are expressed, in terms of
neural structure and function,
can change as a result
of these exposures.
In terms of the stress
response mechanism,
a child born into and raised
in a highly-stressful family
and social environment may
develop an exaggerated stress
response with profound
potential effects on behavior,
both in childhood and, later,
in adolescence and adulthood.
This brings up two
important questions
that we discussed at the
end of the previous lecture.
First, if by adolescence
a child has developed
certain key neural pathways
in a dysfunctional manner,
is it too late to alter them
to a more functional state?
And also, can that
child still learn
new things and new ways of
behaving once he or she becomes
an adult?
As with the previous
lecture, the answers
here suggest that the process
of brain plasticity-- that
is the subsequent altering of
the neural structures developed
during childhood-- that
plasticity is ongoing,
giving each person the
potential to change
both neural structures
and patterns of behavior
internalized as
System 1 thinking.
That potential may slow
down as adults age,
but it does not go away.
This suggests that, even
with those adolescents
and young adults
with some of the most
self-destructive
behavior, the potential
for a positive intervention
with long-term benefits
is still there.
