Biological Explanations of Schizophrenia

Genetic factors

Family studies

They find individuals who have schizophrenia (S) and determine whether their biological relatives are similarly affected more often than non-biological relatives.

They have established that S is more common among biological relatives of a person with S, and that the closer the degree of relatedness, the greater the risk.

Children who have two schizophrenic patients have a concordance rate of 46%, children of one schizophrenic patient 13% and siblings 9%.

(+) Group splitting hypothesis (Stevens and Price, 2000)– Suggest that schizoid personalities performed a valuable function of dividing tribal communities when they became too large. Once a group exceeds its optimum size, splitting the group would increase the reproductive fitness of each individual. S would be an adaptation whose function is to facilitate group splitting. Schizoid symptoms would have led to the splitting of communities and the formation of new ones as these symptoms such as mood changes, bizarre beliefs, hallucinations and delusions of grandeur would induce discontented group members to leave.

(+) Schizophrenia appears to run in families, supporting the argument for a genetic basis for the disorder.

(-) However, many researchers now accept that the fact that schizophrenia appears to run in families may be more to do with common rearing patterns or other factors that have nothing to do with heredity e.g. EE.

Twin studies

These offer a unique opportunity for researchers to investigate the relative contributions of genetic and environmental influences.

If monozygotic (identical) twins, who share 100% of their genes, are more concordant in terms of a trait like S than dizygotic (fraternal) twins who only share 50% of their genes, then this suggests that the greater similarity is due to genetic factors.

(Joseph, 2004) found a concordance rate of MZ twins of 40.4% and for DZ twins of 7.4%.

More methodologically sound studies have tended to report a lower concordance rate MZ twins . However, despite this, twin researchers still argue that even these findings support the genetic position, because they provide a MZ concordance rate that is many times higher than the DZ concordance rate.

 (-) (Joseph, 2004)– However, it is widely accepted that MZ twins are treated more similarly, encounter more similar environments and experience more ‘identity confusion’ than DZ twins. Therefore there is reason to believe  that the differences in concordance rates reflect nothing more than environmental differences.

Adoption studies as alternative- Studies of genetically related individuals who have been reared apart are used because of difficulties disentangling genetic and environmental influences.

(+) (Tienari et al., 2000)– found that 6.7% of the adoptees whose biological mothers had been diagnosed with S, also received a diagnosis. Compared to just 2% of the control adoptees. They concluded that these finding showed the genetic liability to S had been ‘decisively confirmed’.

(-) It is assumed that adoptees are not ‘selectively placed’. However, (Joseph, 2004) claims that this is unlikely. In places like Denmark and the US, potential adoptive parents would have been informed of the genetic background of children prior to selection.

The dopamine hypothesis

States that messages from neurons that transmit dopamine fire too easily or too often, leading to the characteristic symptoms of S.

Schizophrenics are thought to have abnormally high numbers of D2 receptors on receiving neurons, resulting in more dopamine binding and therefore more neurons firing.

Dopamine neurons play a role in guiding attention, so disturbances in this process may well lead to the problems relating to attention, perception and thought found in people with S.

(+) Amphetamines– Dopamine agonists, stimulating nerve cells containing dopamine causing the synapse to be flooded with this neurotransmitter. Large doses of the drug can cause the characteristic hallucinations and delusions of a schizophrenic episode.

(+) Antipsychotic drugs– Dopamine antagonists, blocking the activity of dopamine in the brain. By reducing the stimulation of the dopamine system, these drugs eliminate symptoms, such as hallucinations and delusions. (Davis et al., 1980)– found that when parts. where given either an antipsychotic drug or placebo, the relapse rate of the placebo’s were 55% compared to only 19% of those on the drug.

(+) Parkinson’s disease– Low levels of dopamine are found in people who suffer from Parkinson’s disease, a degenerative neurological disorder. It was found that some people who were taking the drug L-dopa to raise their levels of dopamine were developing schizophrenic type symptoms.

(-) Cause and effect? (Haracz, 1982)– found that pf the most post-mortems studied who showed elevated dopamine levels had received antipsychotic drugs shortly before death. Post-mortems of schizophrenics who had not received medication showed normal levels of dopamine.

(-) A problem is that drugs used to treat schizophrenia by blocking dopamine activity can actually increase it as neurons struggle to compensate for the sudden deficiency.