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An outline and evaluation of the strengths and limitations of neural and biological explanations for Obsessive-Compulsive Disorder (OCD). It covers genetic hypotheses, methods of investigation, candidate genes, neural explanations, and neurotransmitters. The document also discusses the limitations of these explanations and the role of serotonin in OCD.
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Genetic hypothesis
Candidate genes-
genes which create a vulnerability to OCD
5HT1-D beta is implicated in the efficiency of transport of serotonin across synapses
Polygenic
several genes are involved
Taylor (2013) (meta-analysis)
230 different genes may be involved in OCD
Different types of OCD
The origin of OCD has different causes
One group of genes may cause OCD in one person and another group of genes may cause the disorder in another person = aetiologically heterogeneous
Different types of OCD may be the result of particular genetic variations
Neural explanations
Strength
Supporting evidence for the genetic hypothesis of OCD.
Lewis (1936) Assessed OCD patients and found that 37% had parents with OCD; 21% had siblings with OCD. Nestadt (2000); 11.7% concordance rate between OCD sufferers and their first degree relatives, compared to a 2.7% concordance rate across the general population. Miguel (2005), found that identical (monozygotic) twins have a 53-87% concordance rate whilst non identical twins (dizygotic) have a 22-47% concordance rate.
Validates and increases our confidence in the genetic hypothesis for OCD
Furthers our understanding into the genetic influence of OCD
Limitations
Methodological issues with twin studies, it is difficult to separate the genetic and environmental factors in MZ twins, MZ twins may have exactly the same environment unlike DZ who are male and females and likely to be socialised differently (gender socialisation). This could affect the validity of the genetic hypothesis as it is likely that a shared environment will act as a confounding variable. For this reason it is important to consider that OCD may not be 100% genetic. This is further emphasised by the diathesis stress model which claims that genes leave some people more vulnerable to a psychological disorder like OCD but it is not certain they will develop it without being exposed to a stressor. This is evident from Cromer et al (2007)who found that over ½ OCD patients had traumatic events in their past and OCD was more severe in those with more than one trauma
Additionally stating that OCD may be polygenic lowers the predictive validity of OCD as no one candidate gene has been identified as causing OCD. This is a limitation as there are many possible genes, therefore it is unlikely to be useful.
Genetic hypothesis
Candidate genes-
genes which create a vulnerability to OCD
5HT1-D beta is implicated in the efficiency of transport of serotonin across synapses
Polygenic
several genes are involved
Taylor (2013) (meta-analysis)
230 different genes may be involved in OCD
Different types of OCD
The origin of OCD has different causes
One group of genes may cause OCD in one person and another group of genes may cause the disorder in another person = aetiologically heterogeneous
Different types of OCD may be the result of particular genetic variations
Neural explanations
The genes associated with OCD are likely to affect levels of neurotransmitters as well as structures of the brain
Serotonin
Decision making system