Schizophrenia- explanations- biological Flashcards
genetics
we inherit 50% or our genes from each parent, genes code for proteins that create our brains and the neurological networks that make up our mental states including psychopathology. so SZ can be inherited
diathesis stress model
genes- the diathesis- put someone at risk and the stress is the environment that determine who develops the disorder and when. until the 1960s researchers believed sz to be wholly genetic but in recent years it is believed there is an interaction effect. those without the genes will not develop the disorder no matter the environment but those with the genes are affected by environmental stressors.
liability threshold model
behavioural geneticists behaviour that there are a number of genes that are involved in SZ- some possessing greater effect than others. the more of these genes the individual possesses the greater risk of SZ.
prior to this model sz was believed to be caused by a single gene, others have thought that several genes in combination were the sole cause.
combining the diathesis stress model and liability threshold model
those with a higher liability threshold will be more at risk at developing SZ as it will require fewer stressors to trigger onset, whilst those with lower liability threshold require greater or more major stressors for onset (which can be protected against with the right knowledge)
twin studies outline nature of them
if genetics are important
expect higher concordance rates in MZs than DZs because they share all the same genes whereas the later share only half.
natural experiment
IV: degree of genetic similarity
similarity of parenting is controlled within each pair of twins the parental behaviour is likely to be similar
adoption studies outline nature of them
if genetics are important
expect higher concordance rate between adopted offspring of parents with Sz and their biological parents
usually theres a control group of adopted offspring of parents without SZ for possibility that adoption itself can contribute to SZ
separated twin studies outline nature of them
if genes important
concordance between separated MZs should be high
anything above baseline rate (1%) the higher the influence of the genes
molecular genetics outline
if genes important
expect to identify specific genes that increase risk of SZ
likely to be a number of genes
may act in isolation or combination leading to different combinations of symptoms
twins studies results and examples
(and 1 sep twin stud)
bullet point PPE
twin studies show genetic component of SZ and nearly all studies show that MZ twin concordance rates are higher than DZs. e.g.
gottesman review
meta analysis essentially (pooled results from 40 twin studies)
40 paris of twins
pooled concordance rate for MZs was 48% and the DZs 17%
gottesman also did a seperated twin study for 14 pairs of twins MZ concordance was 58%
Very small study but is consistent with findings of other twin studies
Kendler
MZs 53%
DZ 15%
overall and from recent findings
mz twins generally 41-65%
Dz twins generally 0-28%
since this evidence comes from a number of meta-analyses is it particularly strong- the results are less likely to be flukes because they’ve been pooled from large number of studies and MZ and DZ twins and conducted at different times in different studies thus providing strong and consistent support for the genetic explanation.
consistent evidence from a series of reviews for a strong genetic effect
however as genes are clearly not the only factor (never 100% concordance) provides room for environmental effect- for example int he diathesis stress model
Adoption studies results and examples
bullet point PPE
tienari et al
Finnish adopted children who had SZ mothers had a 7% chance of developing sz compared to 1.5% of the controls (who were adopted children without SZ mothers)
the risk for developing sz was 4 times greater for adopted children with SZ bio mothers than it was for adopted children without SZ bio mums
adoptees at moderate-high genetic risk are siginificantly more sensitive to adverse rearing patterns in adoptive families than are adoptees at low genetic risk
fewer adoption studies but they do consistently suggest a moderately strong genetic effect. there is still a high risk of developing sz despite being raised by someone other than the biological mother suggesting it’s genetic
Wahlberg re examined tienari’s findings and found a strong environmental effect for those at risk of developing SZ who were adopted into families with poor communication.
providing direct support for the diathesis stress model of Sz
molecular genetics
research has shown links between a large number of genes which appear to have small effects many of them related to dopamine dysfunction. D2 receptor gene in particular (glut et al)
Allen et al 2008
across a meta analysis 24 genetic variants in 16 different genes (including DRD2) showed to increase risk by 23%
4 of the top 10 gene variants most associated with sz are directly involved in dopaminergic pathways.
a particularly influential gene variant is one that affecting monoamine transporter protein who’s role is to package dopamine and other monoamines into vesicles (an increasing risk of 63%) when this protein is over active it means more dopamine is being released into the synapse and therefore binding to DRD2 receptors on the post synaptic membrane.
providing support for the liability threshold model, as not just one gene is increased and increases in risk are small
methodological issues in research with twin studies
more similar environments for MZs than DZs
may be treated more similarly because they look more alike
it could be that preteens feel more obliged to treat mss similarly because of the perception that they are very similar, whereas this is not he case with DZs
this could therefore mean that there is an environmental reason for the higher concordance rates rather than the genetic reason, which flaws the twin study method (and separated twin method solves)
methodological issues with adoption studies
selective placement
it is possible that children with history of SZ may not be chosen by better informed and potential more contentious parents meaning that those children are instead placed in more psychologically harmful adoptive homes.
this could account for higher concordance rates of s than in control cases, children with S parents may be placed in homes which are more stressful therefore more likely to develop sz
the similarly of the offspring and the sz mother is therefore better explained the the environmental factors, is this criticism is justifiable. A lot of assumptions have been made in relation to pickiness and quality of parenting. a relationship which may exist in some cases but not all and not to the extent of discrediting the genetic effects
to what extent have the findings on the effect of genetics been triangulated?
a number of different studies: twin adopted sep twin genetics
all shown the same result- genetics play a role
CR higher for MZs in all cases
and specific genes have been identified as creating risk
to what extent have the findings of the effect of genetics been replicated /assessed in MA??
(the best)
twin studies- lots of replication - gottesman review of 40 twin studies
adoption studies - 6 studies
separated twin studies (only 14 pairs which gottesman collected) (the worst)
molecular genetics provides vast evidence as this is more objective.
