biological explanations Flashcards
outline the dopamine hypothesis
explain
- one of the most enduring theories in psychology
- explores the idea that the brains of schizophrenic people produce more dopamine than others
- consists of three versions, each one more refined than the next in light of new research and evidence
version 1
- emerged from the discovery of antipsychotic drugs and the work of Carlsson and Lindqvist (1957) who identified that they reduced dopamine production in animals
- evidence that schizophrenics have an abnormally high number of D2 receptors
- Comer (2003) found that dopamine neurons affect attention, and so disturbances in this process may lead to issues with perception
version 2
- updated by Davis (1991) due to evidence uncovered that disagreed with Version 1
- he argued that the negative symptoms of schizophrenia (withdrawal, disorganised speech) result from reduced activity in the mesocortical pathway in the brain
- the positive symptoms of schizophrenia (hallucinations, delusions) result from increased activity in the mesolimbic pathway
version 3
- there has been an influx of research since since v2 (over 6,000 articles)
- Howes and Kapur (2009) proposed a 3rd version which links risk factors to increased presynaptic striatal dopaminergic function as opposed to D2 receptor activity
- refined theory that has developed over time and aims to explain the symptoms of schizophrenia through a biological perspective
outline the dopamine hypothesis
research
- Carlsson and Lindqvist (1957)
- Comer (2003)
- Davis (1991)
- Howes and Kapur (2009)
evaluate the dopamine hypothesis
explain
strengths
- deterministic (if we can infer what is going to happen, we can treat it quickly and focus on developing therapies for it. the single, pin-point focus enables us to focus purely on dopamine production and it has been applied in typical antipsychotics)
- research (it is an enduring theory with lots of supporting evidence e.g. Randrup and Munkvad (1966) administered amphetamine to rats which displayed symptoms of catatonia)
- scientific (most psychological concepts are difficult to measure in a scientific or objective way, research using brain scans, highly controlled lab experiments and the researcher is able to manipulate the variables and confidently conclude)
limitations
- deterministic (ignores free will, excusing behaviour and therefore encouraging deviant behaviour. doesn’t question the biological theory and is therefore too simplistic, reducing the disorder to a neurotransmitter)
- methodological issues (the focus on D2 receptors has been questioned recently, it is based on animal studies which have limited usefulness when generalised to the human population
and v3 relies on PET scan data to estimate synaptic dopamine levels)
- nature (favours nature, restricted and potentially ineffective explanation, does not even consider sociological or environmental factors, too simplistic and lacks balance and NICE suggest CBT as well, lacks self report detail and insight)
evaluate the dopamine hypothesis
research
- Randrup and Munkvad (1966)
outline the cannabis influence on brain chemistry
explain
- cannabis is a recreational drug containing amphetamine and is the most widely used drug among adolescents
- adolescence is a critical period during brain maturation, in particular the development of the endocannabinoid system
- unprecedented unnatural alterations to this system caused by THC (the psychoactive component of cannabis) may affect brain function and have lasting long term effects
- the interaction between the COMT gene and cannabis use may influence genetic susceptibility (Murray 2005)
- 25% of the population have the val/val variant of COMT meaning that they are more likely to develop psychosis and symptoms of schizophrenia if they abuse cannabis in their teen years
outline the cannabis influence on brain chemistry
research
- Murray (2005)
evaluate the cannabis influence on brain chemistry
explain
strengths
- deterministic (if we can infer what is going to happen, we can treat it quickly and focus on developing therapies for it
The single, pin-point focus enables us to focus on the effect of THC)
- research (Di Forti (2009) smoking higher potency cannabis leads to an increased risk of developing psychosis, supporting the hypothesis that sustained THC exposure can lead to schizophrenia)
- scientific (most psychological concepts are difficult to measure in a scientific or objective way, research using brain scans, highly controlled lab experiments and the researcher is able to manipulate the variables and confidently conclude)
limitations
- deterministic (free will, excusing behaviour and therefore encouraging deviant behaviour, if people chose not to take cannabis, these problems would not arise, val/val variant gene
- reductionist and simplistic (schizophrenia is a complex mental disorder and there are non biological factors involved, reduces schizophrenia to drug use. a holistic approach would be a more suitable explanation)
- nature (favours nature, restricted and potentially ineffective explanation, does not even consider sociological or environmental factors, too simplistic and lacks balance and NICE suggest CBT as well, lacks self report detail and insight)
evaluate the cannabis influence on brain chemistry
research
- Murray (2005)