This is the third in our conversation on past trauma. Last week, we asked the question raised by Charles Nemeroff at the American Psychiatric Association’s 2002 annual meeting: "Is the biology of depression the biology of early trauma?"
Women abused in their childhood, he told the gathering, end up with a sensitized brain system. Among other things, higher levels of the stress hormones CRF and ACTH are found in their cerebrospinal fluid and more CRF receptors are in evidence in the neurons.
One of the greatest breeding grounds of stress and trauma is poverty. Earlier this year, I listened to a 25-online lecture series by Robert Sapolsky of Stanford. Dr Sapolsky is probably the greatest authority on how stress is linked to human behavior. How bad is the daily stress of living in poverty? Try this on for size:
Already by age five, according to Dr Sapolsky, there is a relationship between one’s socio-economic status and the thickness of the frontal cortex and its resting metabolic rate. The frontal cortex has one of the highest rates of receptors for glucocorticoids. Glucocorticoids are the last link in the neuro-endocrine loop known as the HPA axis. In a nutshell:
In response to stress or perceived stress the hypothalamus releases CRF into the short blood vessels leading to the pituitary gland. This primes the pituitary to dump ACTH into the bloodstream. Some of this reaches the adrenal gland, which has stored glucocorticoids for such occasions.
Glucocorticoids prime the brain and the body for fight-or-flight. Every available biological process devoted to long-term maintenance gets diverted to short-term survival. The brain is on hyper-alert, the heart is racing, glycogen is converted into instant-energy glucose, on and on it goes ...
Our bodies were designed to handle occasional emergencies. But throw the switch too many times and the system fails to reset to normal. Body and brain are in a constant state of alert. Chronic stress has been linked to just about every physical malady, whether as a cause, a risk factor, or a triggering event. The brain does not get off lightly, either. Let’s follow the glucocorticoid trail:
Glucocorticoids are flooding into the neural synapses. Among other things, this compromises the reuptake of glutamate. Glutamate is a fast-acting excitatory neurotransmitter that activates neurons. This neurotransmitter works in tandem with GABA, which essentially lets neurons know that it’s okay to chill.
But there is no chilling for a neuron that is being exposed to glutamate bombardment. Among other things, excess calcium enters the neuron, which activates certain calcium-dependent enzymes. This can result in cell atrophy and death. According to Husseini Manji, formerly of the NIMH and now at J&J, mood disorders may be fundamentally “atrophic” (ie from brain cells in physical distress) rather than symptomatic.
Wait, it gets worse. Says Dr Sapolsky, a weakened neuron is in no shape to handle the next crisis. So here we have shrunken or dead neurons, unable to communicate with other neurons. Entire brain systems may fail to boot up properly. We lose our capacity to think and feel and regulate our behavior.