Biological explanations of SZ

Biological explanations of SZ

1. GENETICS

   • Appears to run in families & studies claim that the risk of someone developing SZ is proportional to the amount of genes they share.
     • MZ twins (identical) have 48% risk.
       • DZ twins have 17% risk.
         • Children of 2 affected parents have 46% risk.
           • Grandchildren have 5% risk.
     • Gottesman found in several twin studies higher concordance rates for MZ twins than for DZ twins, supporting the claim that risk is higher if more genes are shared.
       • Concordance rates vary widely depending on the methods used to calculate them.
         • sample sizes are small due to MZ twin occurrence being rare and only 1% chance of SZ occurrence in the population.
           • lowers external validity
       • Assumes that environments of MZ&DZ twins are the same, so must mean greater concordance rates are due to greater genetic similarity.
         • Others point out MZ twins have different environments to DZ twins, often treated as 'the twins' not individuals.
           • Difference in concordance rates may only reflect environmental difference of the twin types.
     • Adoption studies have tried to distinguish effects of heredity from environmental effects.
       • Research found high rates of SZ in individuals whose bio parents had SZ even though they were adopted by healthy parents.
         • Tienari studied 155 adopted children whose bio mothers had SZ. They were compared with a healthy matched group & found 10% had developed SZ compared to 1% from the control.
           • Offers strong evidence for genetic component in development of SZ.
             • However, such studies are plagued by methodological problems such as the bias of the researches in favour of genetic conclusions.

2. DOPAMINE

   • Messages from neurones transmitting dopamine fire too easily & too often.
     • SZ's have abnormally high numbers of D2 receptors so more dopamine binds. They play an important role in guiding attention, perception & thought so disturbance in the functions leads to SZ symptoms.
       • Phenothiazines that block dopamine at the synapse are successful at alleviating symptoms.
         • but they don't work for everyone so dopamine may not account for all types of SZ, suggesting different underlying causes.
       • L-dopa for treating Parkinson's increases dopamine levels, resulting in SZ episodes in the treated individuals, highlighting a link between SZ & excess dopamine.
         • Amphetamines also increase availability of dopamine and have made symptoms worse in those already affected, causing characteristic symptoms such as hallucinations.
           • however, this has not happened to all individuals.
       • This explanations is over simplified and does not take into account that other neurotransmitters such as serotonin and glutamate influence development of SZ.
         • Recent research sees prefrontal cortical dopamine deficits as secondary to altered cortical glutamatergic transmission i.e. glutamate levels may play more important role in onset of SZ.
           • research found glutamate agonists reversed SZ symptoms supporting the glutamate theory & its involvement in SZ suggesting dopamine alone is not responsible.
         • high levels of dopamine were not found in all SZ's & modern anti-psychotic drugs such as Clozapine work effectively against the disorder yet have little dopamine blocking activity
           • second generation atypical drugs that reduce serotonin have been found to be better treatment suggesting that other neurotransmitters may be involved.
         • new theories suggest high levels in mesolimbic dopamine system are associated with positive symptoms & high levels in mesocortical system associated with negative.