Biological explanations of SZ

GENETICS
1. Appears to run in families & studies claim that the risk of someone developing SZ is proportional to the amount of genes they share.
  1. MZ twins (identical) have 48% risk.
    1. DZ twins have 17% risk.
      1. Children of 2 affected parents have 46% risk.
        Grandchildren have 5% risk.
  2. 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.
    1. Concordance rates vary widely depending on the methods used to calculate them.
      1. sample sizes are small due to MZ twin occurrence being rare and only 1% chance of SZ occurrence in the population.
        lowers external validity
    2. Assumes that environments of MZ&DZ twins are the same, so must mean greater concordance rates are due to greater genetic similarity.
      1. 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.
  3. Adoption studies have tried to distinguish effects of heredity from environmental effects.
    1. Research found high rates of SZ in individuals whose bio parents had SZ even though they were adopted by healthy parents.
      1. 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.
DOPAMINE
1. Messages from neurones transmitting dopamine fire too easily & too often.
  1. 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.
    1. Phenothiazines that block dopamine at the synapse are successful at alleviating symptoms.
      1. but they don't work for everyone so dopamine may not account for all types of SZ, suggesting different underlying causes.
    2. L-dopa for treating Parkinson's increases dopamine levels, resulting in SZ episodes in the treated individuals, highlighting a link between SZ & excess dopamine.
      1. 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.
    3. This explanations is over simplified and does not take into account that other neurotransmitters such as serotonin and glutamate influence development of SZ.
      1. 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.
      2. 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.
      3. new theories suggest high levels in mesolimbic dopamine system are associated with positive symptoms & high levels in mesocortical system associated with negative.

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Biological explanations of SZ

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