Biological Approach To Schizophrenia

The genetic link to schizophrenia is studied through three methods; family, twin and adoption studies. 

Family studies aim to find a link between relatives. If there is a genetic link, it would be expected that closer relatives would be more likely to share schizophrenia compared to other members of the population. 

Kendler Et Al found that first degree relatives of schizophrenics were 18 times more likely to also develop the disorder compared to others.

Twin studies aim to find whether monozygotic twins have a higher concordance rate compared to dizygotic twins, as MZ twins share 100% of their genetics whereas DZ twins share only 50%. 

Joseph found a schizophrenia concordance rate of 40% for MZ twins and 12% for DZ twins. However it must be noted that identical twins are more likely to be treated as the same person due to more intense similarities and so environmental influences cannot be fully ignored.

Tienari et al found that 6.7% of adopted children who had schizophrenic mothers also developed the disorder, compared to 2% of those whos biological mothers were not schizophrenic. However it has been pointed out that selection bias may have influenced the adoptions. 

The dopamine hypothesis suggests that dopamine receptors fire too easily or too often, resulting in the characteristic symptoms of schizophrenia. New theories suggest that high levels of dopamine in the mesolimbic system are associated with positive symptoms of schizophrenia whereas high levels in the mesocortical system are associated with negative symptoms.

Iverson studied post-mortems of schizophrenics and found high concentrations of dopamine in the limbic system. However it is unclear whether this is the cause or effect of schizophrenia. 

Healy argued that pharmaceutical companies are keen to see this hypothesis promoted as it allows them to make profits off of drugs that lower dopamine levels.

Antipsychotic drugs, the first of which was Chlorpromazine, have allowed many schizophrenics to live normal lives outside of mental institutions. Dopamine antagonists work by blocking the D2 receptors in the synapses that absorb dopamine and thus reducing the positive symptoms of the disorder.

Chlorpromazine does not cure the patient of schizophrenia, instead dampens the positive symptoms to a level where a regular degree of functioning becomes possible. 

Davis performed a meta analysis finding drugs to be 70% successful in improving conditions after 6 weeks, compared to fewer than 25% of schizophrenics improving with the use of placebos. 

Hill highlighted the concern of side-effects. One of which, tardive dyskinesia, affects around 30% of people taking antipsychotics and is irreversible in 75% of cases. This lowers the appropriateness of drug therapies. 

Ross and Read argue that being prescribed medication reinforces the view that there is 'something wrong' with the patients. They argue that this prevents the individual from recovering successfully as they lose motivation.

Electroconvulsive therapy was first used by Cerletti under the false assumption that inducing an epileptic fit would remove the disorder as researchers believed epilepsy and schizophrenia could not co-exist. Although proven to be more effective than placebos, ECT is not as effective as drug treatments. It is not fully understood how ECT affects schizophrenia. 

Tharyan reviewed 26 studies of ECT used to treat schizophrenia, and found that drugs were more effective and therefore more appropriate. 

The main issue with ECT is the ethical concerns raised by the therapy. In the short term, it can cause confusion, memory loss, brain damage, broken bones due to convulsions and even death. A therapy that results in death is inappropriate.