Task 3: childhood stress Flashcards
anxiety disorders
- usually chronic, high occurrence before adulthood
- high comorbidity with different anxiety disorders, also other psychiatric disorders
- highest comorbidity with depression
- early intervention may lower risk for onset, persistence, severity of secondary disorders
- response resembles reactions of normal subjects to conditioned fear cues
Genetics and anxiety disorders
- children with a.d. most likely have parents with a.d.
- genes and environment may be more or less influential depending on developmental stage & quality of primary caregiving
HPA-axis sensitivity programming
- environment can lead to permanent alterations
- maternal care as mediator in regulation of HPA
- good care -> reduced cortisol, attenuation (Verminderung) HPA responsiveness
effects of prenatal anxiety on HPA
- prenatal maternal anxiety: associated with cognitive, behavioral, emotional problems in child
- prenatal cortisol level linked with impaired cognitive development in children
- > BUT: moderated by attachment: negative outcome only when insecure attached
limbic-prefrontal system in anxiety disorders
-elevated activation in limbic structures
-hypoactivation in prefrontal regions aimed at normalizing limbic response
-increased amygdala activation provoked by anxiety-producing stimuli
-prefrontal-amygdala circuit probably mediates mechanisms involved in anxiety
-
attentional bias to threat
- attentional bias associated with heightened HPA activity
- can shape stress responsively and risk for a.d.
early adversity & a.d.
- childhood anxiety predicts occurrence of negative events and negative events predicts anxiety
- secure attachment can act ad protective factor
parenting (modeling and info transfer) and a.d
- parents display of anxiety/verbal behavior emphasizes threat in environment
- > this modeling may be a failure in attachment style: parent doesn’t show appropriate care behavior within a stressful situation, fails to co-regulate child’s stress
parenting style and a.d
- lack of warmth and rejecting behavior -> reinforces believe that world and people are hostile and unsupportive
- over-controlling/rejecting: engender anxious style of attachment
mentalizing and stress
- Effective affect regulation -> reduced reliance on external cues of safety & calling upon mental representations of internalized attachment figures -> internal working models
- Mentally drawing upon past experiences in which stress was effectively co-regulated
- secure attachment can predict ability of theory of mind
mothers mentalizing abilities
= ability to treat child as an psychological agent with mental states independent of their own -> predicts secure attachment and child’s capacity to mentalize
secure attachment and HPA
-> adaptive hypoactivity
broaden and build
- secure attachment leads to seeking supportive attachment relationships throughout the life span
- directs individuals into new environment (broaden) and requires adapting to new challenges (build)
-if insecure attached: coping strategies associated with hyper vigilance prohibit ability to broaden&build
Buffers against stress
- secure attachment: adaptive allostasis and neural plasticity
- capacity to retain high levels of mentalizing when faced with threat/anxiety: keeping regulatory brain regions (PFC) engaged during experience of stress and attachment activation
insecure attachment and stress regulation
- infants use secondary strategies: hyperacttivating (gain attention) and deactivation of modes of stress and anxiety
- anxious attachment: associated with internalizing problems, predisposes to a.d.
- anxious attached: under-recruit PFC involved in emotion regulation
- bias toward negative memories
- amygdala hyperactivation to negative social events
allostatic load
- wears and tears out the body
- emotional regions of brain (fronto-limbic circuit): editor of allostatic load
effect of allostatic load on neural circuits
-can damage circuits due to overproduction of neurochemicals involved in stress response
slow vs reflective response to stress
-Sustained hyperactivity: linked to switch in activation from cortical to subcortical brain systems, from slow, reflective regulation, to a rapid, reflexive response
5HTTLPR - seretonin transported gene polymorphism
- infants SS: more fear
- Strong links between 5-HTTLPR genotype and endophenotypes of depressive disorders like amygdala reactivity, structure & connectivity of the amygdala, ACC and PFC
interaction of 5HTTLPR genotype with quality of maternal care
- insecure attached, ss: 8&12 months: most fear, incline in negative affect expression, decline in positive emotionality
- secure, ss: no high fear at 8m, but at 12m similar level as insecure
- Infants with ss are probably more susceptible to inadequate maternal care
5HTTLPR by environment interaction for anxiety sensitivity
- Interaction between childhood emotional (or physical) maltreatment and 5 HTTLPR genotype
- SS individuals with higher levels of maltreatment had significant higher levels of AS
maternal stress/anxiety/depression and glucocorticoid treatment during pregnancy
-lower birthweight, smaller size of baby
-increased HPA activity
-disturbances in child development and behavior
(unsociable, ADHD, sleep disturbances, psychiatric disorders = depressive symptoms, drug abuse, mood/anxiety disorders)
lower birthweight + lower levels of maternal care
reduced hippocampal volume in adulthood
full-day care centers
- glucocorticoid levels rise in children over the day, more so in toddlers than in older preschool-aged children
- if also less supportive care = larger increases, especially for children who are more disorganized and emotionally negative
- poor care for long hours early in development have increased risk of behavioral problems later
