Brain Story Certification: Module 5

The following information was collected from the Alberta Family Wellness Initiative (n.d.) in module 5.

“Toxic Stress” – Alberta Family Wellness Initiative

• Negative stress weakens the brain architecture
• Adrenaline and Cortisol are two of the hormones involved in the stress response.
• Positive stress is normal and beneficial.  It is short, and not severe stress.  It prepares the mind and body for stressful situations later in life.  We develop positive coping skills from these, which benefit us in the long run.
• Tolerable stress triggers a greater stress response (death of a family member, surviving a natural disaster).  Caregiver support can buffer the impacts of tolerable stress and keep the stress under control.  The supports that help keep the stress in check prevent permanent impacts of the stress.  These are categorized as negative events and are events that are unavoidable in life.  All people experience these, so they are the circumstances were individuals support one another.  larger support networks can also help buffer stress.
• Toxic stress takes place when there is repeated exposure to bad situations (abuse, neglect, violence, & other hardships).  Without the support of caregivers, the hormone levels remain in a higher aroused state.  Toxic stress occurs when bad situations that trigger the increased hormone levels take place repeatedly or over a long time.  This impacts brain architecture and health complications later in life.  It can also influence addiction.

Excerpt from “Good, Bad, & Damaging: Stress & Allostatic Load,” Mathew Holl, PhD

• Stress is often defined as a real or perceived threat to an organism’s wellbeing.
• Stress benefits short-term survival, but in our current social structures does not serve the same usefulness.
• Two pathways are activated to release hormones in stressful/threatening situations. They modify the functions of bodily systems
  • Autonomic response: activation of the sympathetic nervous system.  This leads to the secretion of adrenaline from the adrenal medulla.  This prepares the body to respond to a threat.
  • Adrenocortical Response: Originates in the hypothalamus, leading to secretion of glucocorticoid hormones from the adrenal cortex (cortisol).
• The stress response functions to:
  • Mobilize stored energy to engage in fight or flight.
  • Increase in blood pressure and heart rate to meet energy demands.
  • Increase vigilance as a means to become more aware of the environment.
  • Traffic white blood cells to prepare to wound healing and modulate inflammation response.
  • Enhance memory consolidation.
  • Suppress higher-order cognitive functions to maintain simple behavioural repositories – become more instinctual.
  • Suppress motivation for rewarding stimuli.
• The biological changes enhance the ability of the organism to perform under adverse conditions temporarily
• There is a negative-feedback system where glucocorticoids inhibit their own secretion CRH->ACTH->Cortisol (Cortisol then inhibiting the release of CRH). This is essentially the HPA-axis.
• Hypothalamus: Master control to the adrenocortical response of stress.  It releases a small protein into the blood that enables glucocorticoid secretion in the adrenal cortex. This ultimately controls the activation and termination of the stress response.
• There is higher-order regulation of the hypothalamus.
  • The amygdala influences the hypothalamus through the associations between stimuli and potential outcomes (is the stimulus threatening, and generating the anxiety/fear response).
  • The prefrontal cortex influences decision-making, regulating impulsive behaviours and mental flexibility.  It helps us gauge previous experiences to predict positive or negative responses.  It can constrain the activation of the amygdala and limit activation of the stress response
  • Hippocampus encodes contextual information and consolidates memory – involved in remembering where something happened.  It decreases activity in the hypothalamus and limits the duration of the stress response.

Excerpt from “Effect of Toxic Stress on Children’s Brain and Behaviour.” Judy Cameron, PhD

• Positive stress: Brief increase in heart rate, mild elevations in stress hormone levels.  Short-term stresses.
• Tolerable stress: Serious, temporary stress responses buffered by supportive relationships. Virtually any stress that buffered by adults with minimal impact on brain development.  What were the impacts on the hierarchy of needs, and for how long?  Very dependent on the buffers in place.
• Prolonged activation of stress response systems without any protective relationships to buffer the impacts.  Any adult could have been a buffer for the child.
• Maltreatment, postpartum depression, and parental substance abuse, and neglect are top sources of toxic stress.

Excerpt from “Stress & Neurobehavioral Development in Childhood.”  Megan Gunnar, PhD

• Newborns have a very reactive HPA-axis, and it takes little to elevate the cortisol in newborns.
• The reactivity of the HPA-axis decreases over the first year.  The buffering of the HPA-axis is done through the relationships the infant has with caregivers.
• It becomes harder to get the stress-response system to activate (release of adrenaline), even when the child is placed in experimental situations aimed to increase stress.
• There may be an impact by relationships (secure attachment) on buffering the activation of the stress response system.  Insecurely attached children had an increased salivary cortisol level in a novel situation.  The expectation of support may influence activation.

Excerpt from “Good, Bad & Damaging: Chronic Stress & Allostatic Load.” Matthew Hill, PhD

• Allostasis: Stability through change.
• Allostasis is thus a response that is launched to maintain a normal function within the body system.  This keeps the body in optimal conditions for the environmental demands
• Changes that take place from stress are intended to aid in the survival of the organism.
• Allostatic load is the cost the body endures to keep the body responsive to repeated exposure to stress.  A stress response is meant to be a short-lived process.  Persistent stress results in a breakdown of systems – increasing the wear and tear on the body.
• Acute Stress
  • Increased blood glucose.
  • Increased blood pressure.
  • Modulation of the immune response.
  • The reduced motivation for rewarding stimuli.
  • vigilance and arousal.
  • Consolidation of aversive memories
• Effects of persistent acute stress
  • Excessive insulin secretion: type II diabetes.
  • Hypertension, coronary heart disease.
  • Vulnerability to inflammatory diseases.
  • Loss of interest, & depression.
  • Hyperarousal and anxiety disorders.
  • A preponderance of aversive memories (think of PTSD).
• Allostatic responses over a long period of time increase the vulnerability to the above conditions.
• The brain is also a target of allostatic load from stress/stress hormones through the release of excitatory neurotransmitters.
• Chronic exposure, repeatedly leading to a release of excitatory neurotransmitters, would lead to repeated excitation of neurons.  This becomes toxic to neurons.  Does it lead to the downregulation of the excitatory neurotransmitter receptors? – this may be worth looking into further, as it is not discussed in the video.
• From excessive excitation, neurons retract their dendrites.  Neuronal “shrinkage” is an adaptive response to prevent neuronal death from over-excitation.  This is a very reliable phenomenon across a wide variety of species.
• Neuronal shrinkage leads to neurons no longer functioning optimally.
• This phenomenon has been documented in the hippocampus and prefrontal cortex.
• This leads to memory deficits and the compromised function of the hippocampus, from chronic stress, has adverse effects on memory processes.  This is the cost of the adaptive response.
• Compromised function in the prefrontal cortex influences decision making, poor impulse control, and unhealthy habits that follow chronic stress.  Movement from organized to habitual patterns of behaviour (eg. smoking, over-eating).
• The prefrontal cortex and hippocampus are involved in the perception and termination of the stress response. Therefore, impairments to these structures perpetuate allostatic load, by making it more difficult to alleviate the systems triggering the stress response.
• Thus, and increased perception of stress remains while there is an impaired termination of the stress response.
• Neuronal shrinkage is reversible in the adult brain after the stressor has been removed.
• There is a high degree of plasticity that allows the adult brain to bounce back from the effects of chronic stress.
• repeated exposure to subsequent stressors may decrease the adult brain resiliency, however.

Excerpt from “Residual effects of early life stress into adulthood.” Matthew Hill, PhD

• Early life stress increases the propensity for the development of mental illness and physical diseases.
• Early life stress may change the baseline in which the body responds to or perceives stress.  This can lead to a steady static level of increased stress.
• Early live adversity increases physiological responses to stress.
• Think of the ACE study.
• People who experience childhood neglect/emotional maltreatment have a heightened neural response for fear/anxiety.
• Women exposed to childhood abuse exhibit dramatic elevations in neuroendocrine responses as adults – especially if experiencing depression.
• Individuals who experienced childhood maltreatment also exhibit an increased inflammatory response to stress exposure.
• Early life stress associated with a reduced volume of hippocampus and prefrontal cortex – contributing to sensitization to stress response and reduction in their inhibitory role.
• Evidence points to glucocorticoid resistance when there is early life stress.  This resistance impairs the functions of glucocorticoids.  This is a major theory in the impacts of stress early in life on the lifetime effects on mental and physical health.
• Regulation of inflammatory pathways and CRH by glucocorticoids impact glucocorticoid resistance.
• Glucocorticoids act on white blood cells, reducing the inflammatory molecules.  This then helps limit the inflammatory responses that are induced by stress.
• Resistance to glucocorticoids in white blood cells results in an increase of inflammation on a systemic level in the body.
• Individuals who experience ACE exhibit resistance to anti-inflammatory actions of glucocorticoids.
• CRH released in the hypothalamus leads to the release of glucocorticoids.
• CRH also exists in other brain regions involved in emotional processing and can elicit behavioural changes similar to depression and anxiety.
• CRH may be upregulated in individuals with depression and anxiety disorders.
• Resistance to CRH inhibits the negative feedback loop of the HPA axis, reducing the ability of cortisol to inhibit the system.
• Ages 6-13 appear to have the most significant impacts on CRH sensitization when there is sexual abuse.
• Early life stress impacts glucocorticoid resistance through epigenetic regulation of the glucocorticoid receptor.
• The chemical markers on the gene can either increase the production of the gene’s corresponding protein or decrease the production of the corresponding protein.
• Early life stress adds chemical markers to the gene preventing the rate of gene transcription.  Silencing the transcription of the gene usually persists throughout life.

References

Alberta Family Wellness Initiative. (n.d.). Brain story certification.  Retrieved from https://training.albertafamilywellness.org/