Development, Environment, and Trauma

Question 1

‘Use It or Lose It’

Answer 1

Born with 86 billion neurons, that’s your lot

Initially, hardly any connections -> synapses sprout madly for two years -> then are pruned

Question 2

Grey vs White Matter

Answer 2

Grey matter = cell bodies
White matter = axons + myelin

Always a greater volume of grey than white

Question 3

Dendritic Sprouting

Answer 3

Grey matter volume increases in first few years of life as connections are made

Question 4

Cortex Thinning

Answer 4

From primary school age, cortex thins as it matures, bc:

1) pruning
2) displacement by expanding white matter i.e. myelination, continues into adolescence

Grey matter volume ⬇️ White matter volume ⬆️

Question 5

Environmental Influences on: Cognition

Answer 5

Performance on loads of obvious cognitive tasks (esp. involving executive function and inc. IQ) are affected by environmental variables

Enriched childhood environment (high degree of novelty) –> ⬆️ performance as adult

Childhood trauma and/or abuse (verbal/physical/sexual, neglect) –> ⬇️ performance as adult

Socio-economic status (SES) correlates with:

i) environmental enrichment
ii) longer period of dependency
iii) IQ and other cognitive test performance

Question 6

Environmental Influences on: Mental Health

Answer 6

Low SES, childhood trauma and/or abuse both correlated with increased risk of substance use disorders, depression, suicide etc.

Degree of abuse correlates with extent of mental illness

Anything before 12 years old is especially damaging

Question 7

Environmental Influences on: Brain Maturation

Answer 7

High SES: delayed cortical maturation (both thickening and esp. thinning stages)

Therefore, presumably stress accelerates cortical maturation

Low SES and/or trauma:
- ⬇️  volume of left hippocampus?
- ⬆️  cortical thickness in ventral medial PFC
- ⬆️  / ⬇️  amygdala size?
Data is messy and inconsistent

Question 8

Hypotheses for Pathophysiology

Answer 8

Allostatic Load
vs
HPA Axis

Question 9

Allostatic Load hypothesis

Answer 9

Chronic stress -> increased ‘allostatic load’ -> accelerated ageing

(Allostasis: like the balance of homeostasis, but with too much weight (stress) for the scales to manage)

Evidence:

• Kids in low SES i) enter puberty earlier, ii) have increased cortisol and iii) show faster accumulation ageing biomarkers
• Childhood trauma/abuse correlates with adult cardiac ischemia, cancer, lung and liver disease etc.

Question 10

HPA Axis hypothesis

Answer 10

Chronic stress -> over-activation of HPA axis

Hormone release:
CRH (hypothalamus) –> ACTH (pituitary) -> cortisol (adrenal)

Evidence:

• Specific genetic polymorphisms of CRH receptors implicated in stress-related abnormalities
• Medial PFC, amygdala, hippocampus have CRH-receptors: could mediate developmental changes. Possible abnormalities found in all of these structures [see Environmental Influences on: Brain Maturation]
• Early grooming in rats i) impacts expression of glucocorticoid receptors in hippocampus and ii) influences lifelong release of ACTH

Question 11

Diurnal cortisol release

Answer 11

Normal cortisol levels follows a ‘diurnal pattern’: peak approx. 30 min after awakening

Alterations associated with trauma/abuse

But careful: diurnal levels are not a direct measure of stress response, instead an independent measure of HPA axis functioning

Question 12

Protective factors

Answer 12

‘Social buffering’ i.e. support from intimate community

Enrichment of environment (dopamine)
Social binding (oxytocin)

Attachment and Biobehavioral Catch-Up (ABC) trial:
responsive caregiving can mediate cortisol reactivity

Animal models: Maternal interactions -> ⬇️ HPA axis reactivity to stressors

Question 13

Shitty data

Answer 13

Good studies into long-term effects of environment/trauma/abuse are really hard

How can you control for every other variable between groups? Impossible.

Plus, literature so far lacks standardisation (demographics, trauma types, mental illness types)