Cultic Studies Review, Vol. 5, No. 6, 2006, Page 6
faster, and to our muscles, to prepare our bodies either to fight or to run away when we
don‘t think we have a chance of winning the fight. In addition, epinephrine and its
derivative, norepinephrine, are responsible for narrowing attention so that we don‘t get
distracted but are able to bring all our mental faculties to bear on the present danger
(Cozolino, 2002). Obviously, this response has survival value and, thus, has survived
evolutionary modifications over time.
The Hypothalmic-Pituitary-Adrenal Axis
There is a wonderful feedback loop in the brain, known as the HPA (Hypothalmic-Pituitary-
Adrenal) axis, which lets the body know when the danger is over and to return to baseline.
This response occurs when cortisol reaches a certain critical level. When that happens, the
body gets the message that the emergency chemicals are no longer needed, so the body
can relax (Harvard Mental Health Letter, 2002). For example, when we slam on the car
brakes because we almost went through a red light, cortisol levels are elevated in our
bloodstream. Soon afterward, when we catch our breath and realize we are safe and there
are no cops around, the brain sends signals that tell the pituitary and adrenal glands
responsible for cortisol levels that everything is okay, and the body returns to its former
homeostatic state. In this way, we have warp speed when we need it to cope with the crisis,
but we don‘t live there. This feedback loop is important because although cortisol is
necessary in the short-run, it is toxic in the long run. And while epinephrine gets in and out
of the body quickly, as previously mentioned, cortisol is slower to return to baseline and,
therefore, can be harmful to the organism. If left in the bloodstream too long, cortisol
actually burns out synaptic connections in the brain and wears out bodily organs, which can
lead to various illnesses—ulcers, heart disease, and so on. In other words, under chronic
stress, these hormone levels, especially that of cortisol, are turned ON but unable to turn
OFF.
For children who have been maltreated, the problem is that they do, in fact, live in this
chronic state of emergency, and their bodies continue to be ―at the ready‖ to fight or flee.
Initially, adrenaline levels rise more quickly, but cortisol levels fail to reach the critical level
for shutdown. One theory for this phenomenon is that the brains of traumatized people have
fewer cortisol receptors, paradoxically making them less sensitive to knowing when the
emergency is over, and thus leaving them in a highly anxious state (Applegate &Shapiro,
2005). This chronic state of readiness puts a tremendous strain on their bodies. Research
has shown, for example, that traumatized children are from 10 percent to 15 percent more
likely to suffer from cancer, heart disease, and diabetes as adults (see, for example, Fellitti,
et. al, 1998).
The Amygdala
To explain further, the amygdala, a primitive brain structure situated at the top of the brain
stem, ―acts as a sensory gateway to the limbic system‖ (Schore, 2003, p. 236), or
emotional brain. The amygdala can become sensitized to fear and danger. Repeated stress
causes the amygdala to become irritable and reactive, which results in a situation known as
kindling. This is an appropriate term because, just as a small spark can set a whole
neighborhood up in flames, the neurons neighboring an irritable amygdala can be set off
easily. Support for this idea comes from studies of other limbic regions. Teicher, Glod,
Surrey, &Swett (1993) reported increased limbic system activity, suggestive of temporal
lobe epilepsy, in 253 patients who had been physically (38 percent increase) or sexually (49
percent increase) abused as children. Those who had survived both types of maltreatment
had a 113 percent increase in limbic excitation. A very recent study by Teicher, Samson,
Polcari, and McGreenery (2006), which examined the effects of parent verbal aggression, a
less-studied form of child maltreatment, found significant robust effects on measures of
limbic irritability and dissociation among other variables.
faster, and to our muscles, to prepare our bodies either to fight or to run away when we
don‘t think we have a chance of winning the fight. In addition, epinephrine and its
derivative, norepinephrine, are responsible for narrowing attention so that we don‘t get
distracted but are able to bring all our mental faculties to bear on the present danger
(Cozolino, 2002). Obviously, this response has survival value and, thus, has survived
evolutionary modifications over time.
The Hypothalmic-Pituitary-Adrenal Axis
There is a wonderful feedback loop in the brain, known as the HPA (Hypothalmic-Pituitary-
Adrenal) axis, which lets the body know when the danger is over and to return to baseline.
This response occurs when cortisol reaches a certain critical level. When that happens, the
body gets the message that the emergency chemicals are no longer needed, so the body
can relax (Harvard Mental Health Letter, 2002). For example, when we slam on the car
brakes because we almost went through a red light, cortisol levels are elevated in our
bloodstream. Soon afterward, when we catch our breath and realize we are safe and there
are no cops around, the brain sends signals that tell the pituitary and adrenal glands
responsible for cortisol levels that everything is okay, and the body returns to its former
homeostatic state. In this way, we have warp speed when we need it to cope with the crisis,
but we don‘t live there. This feedback loop is important because although cortisol is
necessary in the short-run, it is toxic in the long run. And while epinephrine gets in and out
of the body quickly, as previously mentioned, cortisol is slower to return to baseline and,
therefore, can be harmful to the organism. If left in the bloodstream too long, cortisol
actually burns out synaptic connections in the brain and wears out bodily organs, which can
lead to various illnesses—ulcers, heart disease, and so on. In other words, under chronic
stress, these hormone levels, especially that of cortisol, are turned ON but unable to turn
OFF.
For children who have been maltreated, the problem is that they do, in fact, live in this
chronic state of emergency, and their bodies continue to be ―at the ready‖ to fight or flee.
Initially, adrenaline levels rise more quickly, but cortisol levels fail to reach the critical level
for shutdown. One theory for this phenomenon is that the brains of traumatized people have
fewer cortisol receptors, paradoxically making them less sensitive to knowing when the
emergency is over, and thus leaving them in a highly anxious state (Applegate &Shapiro,
2005). This chronic state of readiness puts a tremendous strain on their bodies. Research
has shown, for example, that traumatized children are from 10 percent to 15 percent more
likely to suffer from cancer, heart disease, and diabetes as adults (see, for example, Fellitti,
et. al, 1998).
The Amygdala
To explain further, the amygdala, a primitive brain structure situated at the top of the brain
stem, ―acts as a sensory gateway to the limbic system‖ (Schore, 2003, p. 236), or
emotional brain. The amygdala can become sensitized to fear and danger. Repeated stress
causes the amygdala to become irritable and reactive, which results in a situation known as
kindling. This is an appropriate term because, just as a small spark can set a whole
neighborhood up in flames, the neurons neighboring an irritable amygdala can be set off
easily. Support for this idea comes from studies of other limbic regions. Teicher, Glod,
Surrey, &Swett (1993) reported increased limbic system activity, suggestive of temporal
lobe epilepsy, in 253 patients who had been physically (38 percent increase) or sexually (49
percent increase) abused as children. Those who had survived both types of maltreatment
had a 113 percent increase in limbic excitation. A very recent study by Teicher, Samson,
Polcari, and McGreenery (2006), which examined the effects of parent verbal aggression, a
less-studied form of child maltreatment, found significant robust effects on measures of
limbic irritability and dissociation among other variables.
