biological explanation - genetics

• schizophrenia may be inherited. contemporary biess suggest that hereditary explains at least 50% of the cause of schizophrenia.

• its very unlikely that there is one gene which causes schizophrenia but possessing a certain combination of genes makes you more susceptible to developing the disorder. (epigenetic)

• evidence on a genetic influence historically came from twin studies and more recently from gene mapping studies

• as monozygotic twins share 100 % of their genes but dizygotic twins only share 50%, if schizophrenia was a genetic disorder you would expect that the concordance rate for mz twins would be greater than for dz.

concordance rate = probability that a pair of individuals with both have a certain characteristic, given that one of the pair has the characteristic.

• gottesman and shields (1982)

conducted a meta-analysis of 5 studies in twins. mz concordance 46 % and dz 14.

conclusion -  as mz twins have greater concordance rates and share more genes than dz twins suggest that genetic may be influencing the development of schizophrenia and this supports the genetic explanation.

• a weakness is that mz twins are often treated more similarly and tend to grow up in more similar environments than dz twins and this may be why it causes higher levels of concordance between them. this offers evidence against genetic explanations as it suggests that environment may be influencing schizophrenia not genetics.

• a weakness is that it has a small sample size of usually 20. so one twin pair will have a large effect on concordance rates. it may affect reliability as it is unlikely there will be many twins and those who will generally take part. there's also not that many twins , so it will be difficult to find out where it all occurs. the sample size isn't representable as it is less likely to be able to generalise to all towns.

• older twin studies may be unreliable due to changes in diagnostic criteria. some people diagnosed 40 years ago may not have been diagnosed today. equally some people not diagnosed 40 years ago may be diagnosed today. it undermines the validity of diagnostic criteria where we may not be able to establish the difference between now and 40 years ago. it is based on unreliable data and unlikely to have a retest reliability. may change the concordance rate and we can not see how reliable the explanation is

• a solution for the argument over whether influences are as a result of environment or genetics

• tienari et al

164 adoptees whose mothers had been diagnosed with schizophrenia, 11 (6.7%) also received a diagnosis of schizophrenia, compared to just 4 (2%) of the 197 controlled adoptees without schizophrenic mothers

• researchers said findings showed that the genetic liability to schizophrenia has been 'decisively confirmed'

• strength of adoption studies is that they provide better evidence with regards to relationships and genetic factors. in contrast, to the retrospective nature of both family and twins studies, prospective studies such as adoption studies can be seen to be more reliable because it follows the same group over a consistent period of time. as a result, we can more comparisons before and after any sign of the illness appeared. kety's study provided support for the genetic causes of schizophrenia. however, because the children share the same environment as their mothers, researchers cannot differentiate between genetic and environmental influences. also, because of the continually changing diagnostic criteria, the results need to be generalised with caution as validity is affected.

• even though it provides strong support for genetic causes, the research of tienari is a good example of the need to interpret results cautiously. for example, where the risk of developing schizophrenia was found to be 4x greater in adopted children with biological mothers diagnosed with schizophrenia than those who were not. wahlberg et al (2000) found that there was a strong interaction between genetic and environmental factors and only adopted children in families with poor communication were at an increased risk of developing schizophrenia. therefore, these adoption studies somewhat undermine the hereditary explanation.

• find families where an individual/multiple members have schizophrenia and determine whether their biological relatives are similarly affected more often than non-biological

• studies have established that schizophrenia is more common among biological relatives of a person with schizophrenia, and the closer they are the greater the risk

• gottesman

children with 2 schizophrenic parents had a concordance rate of 46%, children with 1 schizophrenic parent had a rate of 13%

• gottesman

children with 2 schizophrenic parents had a concordance rate of 46%, children with 1 schizophrenic parent had a rate of 13%

• a weakness with family studies is that most of the research done is retrospective, comparing a group of people who have already been diagnosed which creates a problem of historical validity. this is because other variables present at the time of diagnosis cannot be researched, therefore, given the validity and reliability problems of the classification and diagnosis of schizophrenia according to mojabi, nicholson and whaley, any variation in family studies results might be due to classification and the resultant unreliable or invalid diagnosis, rather than anything else and may therefore be inconclusive.

• further weakness of family studies is that of nature vs. nurture. this is because family variables are not controlled which means that schizophrenia may be due to something else other than heredity. for example, it is generally accepted by researchers that common parenting practices across families could interfere with the results in this type of research. research on expressed emotion has shown that the negative emotional climate in some families may lead to stress beyond an individual's coping mechanisms, thus triggering a schizophrenic episode. since parenting practices could be an intervening variable in gottesman (1991) correlational studies, other sources of research which have more control over the variables are required to increase the validity of results and provide a stronger indication of the role of genetic causes for the onset of schizophrenia. therefore, there is a problem with the research question in gottesman's study because it is not close enough to the proposed cause i.e. genes are a more reductionist approach with greater control over the genetic relationship between the programme participant would be more useful.