Schizophrenia Flashcards
Genetics (2nd)
One dis of using family studies is that most children also share the same environment as their parents and spend more time together so will influence each other’s behaviour. This means we cannot rule out the influence the environment may have on the development of SZ as it is difficult to separate the influence of nature and nurture in a family.
Genetics (3rd)
Despite this criticism, there are many studies which do provide strong evidence for a genetic cause such as Gottesman’s. He found that 46% of children with 2 SZ parents will develop SZ. This likelihood decreases to 16% if only one parent is SZ. Gottesman shows that the concordance rate is much higher between relatives, supporting the influence of genetic factors.
(However, another issue with family studies is that it is a very small sample due to the difficulty of finding families with 2 SZ parents and a SZ child. This means that the findings cannot be generalised to the whole population as they have low population validity)
Genetics (4th)
Using adoption studies is a more effective way of looking at SZ as it allows the researcher to separate the influence of genetic factors from the influence of environmental factors. Kety et al were interested in whether the concordance rate of SZ differed between adopted adults with a SZ biological mother and adopted adults without a SZ relative. They found that the rate of SZ was much higher in people whose biological parent had been diagnosed as SZ, despite being raised by non-SZ adults. This shows that the genetic influence is more significant then environmental factors.
Genetics (5th)
The trouble with using adoption studies is that it is hard to access the reasons behind the child’s adoption but it’s possible that the child suffered some type of trauma which has led to their development of SZ as the diathesis-stress model suggests that stress can trigger the onset of SZ. Similarly, the time they had spent with their SZ parent may have influenced the way they behave. For example, children often copy what they see their parents doing, so imitation of the SZ behaviour could have increased their likelihood of developing the disorder themselves.
Dopamine (1st)
The dopamine hypothesis is another explanation used in the biological approach. This explains that schizophrenia is due to an excess of dopamine (neurotransmitter). This causes the neurons to fire too often, therefore transmitting more messages which is believed to cause the schizophrenic symptoms.
Dopamine (2nd)
Evidence to support this hypothesis comes from the research into antipyschotic drugs which reduce SZ symptoms by blocking the dopamine receptors. This suggests that it is overactive dopamine receptors which cause the symptoms.
L-Dopa is a chemical used to treat people with a lack of a dopamine. It is found that when it is given to patients with Parkinson’s disease, it can produce positive SZ symptoms in the patients, which indicates that dopamine levels are related to SZ symptoms.
Dopamine (3rd)
A weakness with the hypothesis is that it is unclear whether the dopamine levels cause SZ, or if having SZ causes an increase in the level of dopamine. This uncertainty makes it difficult to establish a cause and effect relationship between dopamine levels and SZ.
A second weakness is that if antipyschotic drugs block the dopamine receptors, and the sensitivity of dopamine receptors are the cause of the symptoms, when the drugs are taken there should be a rapid improvement of all the SZ symptoms displayed as antipyschotics block the dopamine receptors. However, this is not what happens and only positive symptoms tend to improve. As well as this, it can be up to 2 months before the antipyschotic drugs start working and an improvement is shown.
Dopamine (4th)
There is also a second version of the DH which states that rather an excess of dopamine, it is claimed that people with a diagnosis of SZ had an excess of dopamine receptors. More receptors leads to more firing and an overproduction of messages.
There is evidence to support this as some autopsies have found an usually large number of dopamine receptors in the brains of SZ, but the evidence is inconclusive..
Brain (1st)
The biological explanation also claims that abnormalities in the structure of the brain can also cause SZ. Research has found that SZ have enlarged ventricles in the brain compared to non-schizophrenics suggesting that SZ is linked to a loss of brain tissue. There are also abnormalities in their frontal lobe which could be the cause of their disorganised thoughts, identified by the use of MRI scanning.
Brain (2nd)
This research is highly reliable as it has to be carried out in controlled environments using specialist researchers and equipment as the study of the brain is very vital. All these factors suggest that the findings of studies would be found by other researchers who carried out the same study.
A limitation of stating abnormalities such as enlarged ventricles in the brain is the cause of SZ, is that if this was the case, no-one would be able to be cured. This is because the brains cortex does not grow back to fill the space of the enlarged ventricles so no one would be able to make any improvements in their condition. Considering this factor, 35% of SZ are classified as being ‘much improved’ later on in life, this shouldn’t be possible if the basis of SZ is the loss of brain matter.
Genetics (1st)
The argument that genes are the cause of schizophrenia, predicts that the rate of SZ will be higher between relatives due to the offspring of a SZ inheriting this gene. The claim is supported by the prevalence statistic being the same around the world at 1% of the population having SZ, showing that the prevalence doesn’t vary with the environment.u
