Lecture 1 - Foetal or prenatal programming Flashcards
(24 cards)
1
Q
How do psychosocial problems develop?
A
- Family influences via genes and good quality family environment, as well combination via interaction
- How do these conditions influence physiological and brain functioning e.g. Biological, cognitive and emotional processes, turn into these behavioural outputs
- Also the factor of individual differences, not all children who face the same factors develop problems, also questions resilience
2
Q
What are three areas of life where there are positive growth but stunting can lead to problems?
A
- Prenatal period
- Early postnatal years
- Adolescence: exuberant growth during these phases gives brain potential
3
Q
What is the Diathesis stress model?
A
- Genetic predispositions and childhood trauma interact and affect the vulnerability to the mental disorder
- If in minimal stress = lower probability of mental disorder and vice versa
4
Q
What is Stress as a bodily response?
A
- Strong, healthy stress response = deal and continue with problems = less vulnerable to mental disorder
- Stress is good as it allows us to be productive and escape danger = allows us to have tunnel vision and not being distracted by thoughts/feelings
- Can be bad sometimes when out of control
5
Q
What is the sympathomedullary pathway?
A
- Quick, instinctive, system 1, automatic
- Fight/flight
- Hypothalamus activates adrenal medulla
- Adrenal medulla releases adrenaline and noradrenaline into the bloodstream
- Cortisol diverts blood glucose to muscles = less glucose for the hippocampus = harder to make memories or remember
- This reinforces the pattern of sympathetic reaction and activates fight/flight
- Nothing to do psychologically
6
Q
What is the pituitary-adrenal system?
A
- Higher brain centres activates hypothalamus
- Hypothalamus releases corticotrophin
- Pit. Gland releases adrenocorticotrophic
- Adrenal cortex releases corticicosteriods
- Causes changes on liver and immune system
- Very costly = knock on affects are dangerous for the body
- Stress systems should not respond when there is no need to
- Cortisol can cause long term damage to immune system and growth hormonal system
- Need a system fit for purpose
7
Q
When is the stress system triggered?
A
- Triggered by amygdala = tells HPA to release cortisol
- When stress is over, there needs to be a system to tell HPA to stop producing cortisol = negative feedback system linked to hippocampus
- Hippocampus reduces impact of stress by decreasing intensity or duration
- Excess cortisol levels activate brains glucocorticoid receptors in HPA axis and hippocampus to suppress production of CRH/stress hormones
8
Q
How is the hippocampus affected by stress?
A
- Cannot access or store or create new memories during stress
- Most damaged area by excessive/prolonged cortisol exposure = damaged hippocampus causes cortisol levels to get out of control - further compromising memory and cognition
9
Q
What are the longer term effects of chronic stress?
A
- We have overactivity of amygdala and underactivity of hippocampus
- Leads to poorer stress control and impaired memory and lower fear conditioning
- Fysiological damage to hippocampal dendritic growth but increased growth in amygdala
- Psychological: Increased anxiety (hypervigilance) and impaired learning and memory (poor memory and retrieval)
10
Q
What are individual differences in psychological states?
A
- Psychological factors modulate the stressfulness of a stressor e.g is it a challenge or stress
- Psychological factors can trigger a stress response in the absence of homeostatic disruption = can make self very stress without risk
- Psychological factors make numerous physical stressors no longer stressful - habituation (e.g loud noise)
11
Q
What is the foetal programming hypothesis?
A
- The prenatal environment provided by the mother has lasting or lifelong significance through endocrine and metabolic processes
- Influences foetal brain development and consequently infant’s cognitive and emotional development during the first months of years of life
- Maternal cortisol cross relatively easily the placental barrier and influence brain development in regions associated with learning, memory and emotional development
12
Q
What is Foetal Programming study?
A
- Emotional state of mother affects child she is carrying
- Prospective studies report that maternal stress/anxiety is associated with adverse obstetric outcomes
- Risk for premature delivery, low birth weight
- Smaller head circumference when corrected for birth weight
- Lower scores obtained at neonatal neurological examination
- During observation we can see when mum is stresses, children have abnormal outcomes
- Stressed monkeys, rats and looked at their offspring = children are more anxious, issues with motor developments, issues with learning
13
Q
What are mechanisms underlying alterations in offspring behaviour and development?
A
- 3 ways to have stress go to baby from mother
- Prenatal stressors activate the maternal HPA-axis and elevate her plasma levels of glucocorticioids
- Results are dysregulation of the foetal HPA axis with chronically elevated levels of circulating glucocorticoids and altered feedback regulation
14
Q
What is transplacental transport?
A
- 11 BHSD is an enzyme in primates that converts cortisol in mother into something inactive = can protect child
- In rodents, corticosterone easily crosses the placenta, human foetuses are relatively protected from this enzyme
- This is an individual difference
- Maternal and foetal cortisol levels are correlated in spite of importance of enzyme and maternal cortisol may account for a large part of variance in foetal concentration
15
Q
What is maternal stress-induced release of placental hormones into foetal circulation?
A
- Maternal stress increases production of stress hormones by placental cells = in primates only
- Leads to pre-term delivery and growth retardation
16
Q
Maternal stress-induced effects on blood flow to placenta?
A
- Maternal stress activation of SNS could reduce utero placental blood flow which hampers the transport of oxygen and nutrients to foetus and impair development
- Leads to foetal stress
17
Q
What are HPA axis changes in prenatally stressed offspring?
A
- The ultimate effect of maternal and placental stress hormones entering foetal circulation is by affecting foetal hippocampal ontegeny
- Receptor down-regulation in hippocampus
- Exertion of neurotoxic effects on hippocampal cells
- Decreased sensitivity of glucocorticoid receptors at any level in HPA axis
18
Q
What did O’Connor say?
A
- Human studies on effects of antenatal stress on child outcome and behaviour have methodological problems
- Small sample sizes
- Lack of stat control: stress can be various in size and direction
- Reliance on retrospective reports: unreliable
- Failure to distinguish between prenatal and postnatal stress as some same stresses will occur before and after pregnancy
19
Q
What was prospective research by O’Connor et al?
A
- Sample based on ALSPAC study
- Measures: maternal anxiety and depression were measured at 18 wks and 32 wks and postnatally
- Looking at child measures via emotional and conduct problems
- Anxiety at 32 wks are more likely to have hyperactivity problems with boys, conduct problems with boys, and equal problems emotionally in boys and girls
- No effect of postnatal depression
- Mothers who scored in the top 15% of the sample on anxiety at 32 wks gestation were more likely to have a child who scored more than 2sds over the mean in behavioural/emotional problems
- Suggests that antenatal prediction is not mediated by a link between antenatal and postnatal anxiety or depression but is due to a direct causal mechanism operating in the antenatal period.
- All maternal report - critique - not objective of bio processes
20
Q
What was prenatal depression effects on neonates?
A
- Prenatal depression is common, under-recognised and under-treated
- Infants of depressed mothers show depression-like behaviours from birth, prior to experience interacting with the mother such as flat affect, lower activity, greater irritability, inferior orienting and motor tone and inferior performance on Brazelton Assessment
21
Q
What was a study looking at prenatal depression?
A
- 63 Pregnant women = 36 with elevated depression scores
- Looked at maternal stress & depression, foetal attachment scale and DIS
- Brazelton Neonatal behaviour Assessment 1 week after birth = neurobehavioural exam
- High depressed and low in mother had significantly higher levels of cortisol, but 24 hr after, differences went away
- In babies this prenatal pattern was reflected in cortisol
- Seen in dopamine, epinephrine and norepinephrine
- Children had behaviourally/neurological effects in high risk children - did less well with reflexes and their interactions with the tester = pattern of elevated risk
22
Q
What are the implications of the study?
A
- Sympathetically aroused state of newborn and less optimal neuro behaviour is worrisome given their risk for being less interactive because of being parented by depressed mum
- Bidirectional process: already sympathetically aroused infant may further depress mother and make it hard to establish satisfying relationship with infant
23
Q
What were the studies about COVID and pregnancy?
A
- No effect of having covid and neurodevelopment of children
- When comparing whole cohort of mothers and children
- Cohort of children are negatively affected
- Stress of covid more generally has had a negative effect on children
24
Q
What were key findings of neurotransmitter system alterations?
A
Offspring of prenatally stressed animals exhibit reduced activity in the opioid, GABA, serotonin and dopamine systems
