Biological explanations for schizophrenia Flashcards
What have family studies shown?
Biological explanations
Risk of SZ increases in line with genetic similarity to a relative with the disorder.
Gottesman (1991)
Biological explanations
Large-scale family study
Findings - someone with aunt with SZ has a 2% chance of developing it, increasing to 9% if individual is a sibling adn 48% is they are an identical twin.
Candidate genes
Biological explanations
SZ appears to be polygenic
Most likely genes would be those coding for neurotransmitters like dopamine
SZ also likely to be aetiologically heterogenous - diff combos of factors can lead to condition
Ripke et al (2014)
Biological explanations
Combined all previous data from genome-wide studies of SZ
Genetic make up of 37,000 people with a SZ diagnosis was compared to 113,000 controls.
108 seperate genetic variations were associated with slightly increased risk of SZ
Mutations
Biological explanations
Caused by radiation, poision or viral infection
Brown et al (2002) - Evidence for mutation comes from posotive correlations between paternal age (increased risk of sperm mutation) and risk of SZ, increasing from 0.7% in fathers under 25 to over 2% in fathers over 50
Research support
Biological explanatons
Strength
Family studies such as Gottesman show that risk increases with genetic similarity to a family member with SZ. Adoption studies (Tienari et al (2004)) show bio children of parents with SZ are at higher risk even if raised in adoptive family. Twin study by Hilker et al (2018) showed concordance rate of 33% for MZ twins and 7% for DZ
Shows some people are more vulnerable to SZ as result of genetic make up
Environmental factors
Biological explanations
Limitation
Include both biological and psychological influences. Bio rish factors include birth complications (Morgan et al 2017) and smoking THC-rich cannabis in teen years (Di Forti et al 2015). Psycho risk factors include childood trauma which leaves people more vulnerable to adult mental health issues. Morkved et al (2017) - 67% of people with SZ and related psychotic disorders reported at least one chillhood trauma as opposed to 38% of a matched group with non-psychotic mental health issues.
Means genetic factors alone cannot provide complete explanation for SZ
Genetic counselling
Biological explanations
If one or more potential parents have a relative with SZ , they risk having a child who could develop SZ
However, risk estimate provided by genetic counselling is just an average figure. Won’t reflect probability of a particular child going on to develop SZ because they will experience a particular environment which also has risk factors.
Original dopamine hypothesis
Biologucal explanations
Seeman (1987) - discovery that drugs used to treat SZ caused symptoms similar to those in people with Parkinson’s disease (condition assocaited with low DA)
Therefore, SZ may be result of hyperdopaminergia in subcortial areas of brain (e.g. excess of DA receptors in pathways from subcortex to Broca’s may explain symptoms such as speech poverty or auditory hallucinations
Updated dopamine hypothesis
Biologucal explanations
Davis et al (1991) proposed addition of cortical hypodopaminergia. Can explain symptoms of SZ (e.g. low DA in prefrontal cortex could explain cog problems (- symptoms)).
Also been suggested cortical hypodopaminergia leads to subcortical hyperdopaminergia.
Current versions of dopamin hypothesis try to explain origins of abnormal DA function.
Howes et al (2017) - seems both genetic variations and early experiences of stress make some people more sensitive to cortical hypodopaminergia and subcortical hyperdopaminergia
Evidence for dopamine
Biological explanations
Strength
Curran et al (2004) - Amphetamines increase DA and worsen symptoms in people with SZ and induce sumptoms in people without.
Tauscher et al (2014) - antipsychotic drugs reduce DA activity and reduce symptom intensity
Some candidate genes act on production of DA or DA receptors
Suggests that dopamine is involved in symptoms of SZ
Gultamate
Biologucal explanations
Limitation
Post-mortem and live scanning studies consistently found raised levels of glutamate in several brain regions if people with SZ (McCutcheon et al 2020)
Several candidate genes for SZ are believed to be involved in glutamate production or processing
Means an equally strong case can be made for other neurotransmitters
Amphetamine psychosis (dopamine hypothesis evaluation)
Biological explanations
Tenn et al (2003) induced SZ-like symptoms in rats using amphetamines, then relieved symptoms using drugs that reduced DA action (supports DA hypothesis)
However, other drugs that increase DA (e.g. apomorphne) don’t cause SZ-like symptoms (Depatie and Lal 2001)
Garson (2017) challenged idea that amphetamine psychosis closley mimics SZ
