The importance of genetic factors also emerged in two studies that investigated the risk of schizophrenia among offspring of identical twins discordant for schizophrenia (Gottesman et al, 1982, Kringlen and Cramer, 1989). In the Danish twin study there was no significant difference in the risk of schizophrenia between offspring of affected twins (10%) and unaffected co-twins (17%) (Gottesman et al, 1982). However, sample sizes were quite small: three schizophrenic twins had a total of 14 offspring, 1 of whom was affected; while 6 unaffected co-twins had 24 offspring, 4 of whom were affected.
The sample size in the Norwegian twin study was larger (Kringlen and Cramer, 1989). Of the 28 offspring of schizophrenic twins, five (18%) developed the disorder; whereas 2 of the 45 offspring of unaffected co-twins had schizophrenia. These differences were not statistically significant. Although both of these studies lacked statistical power, they suggest that unaffected MZ co-twins tend to carry the genotype predisposed to schizophrenia; but that it remains unexpressed in them - for example, because they have not been exposed to environmental risk factors (Gottesman et al, 1982).
Twin studies, in summary, suggest that genetic factors are the most important risk factors for schizophrenia. However, environmental factors are also important, as less half of individuals with an identical genome - identical twins- are concordant for schizophrenia.
Adoption studies compare the effect of different rearing environments among groups that are assumed to be similar in their genetic predisposition, and the effects of different genetic predispositions among groups that are assumed to have similar rearing environments.
In the adoptees’ family design, the group of adoptees who have developed schizophrenia in adulthood and unaffected control adoptees are compared. The psychiatric status of the biological and adoptive relatives is investigated. If genetic factors are important,, the rate of schizophrenia should be higher among the biological than adoptive relatives of an affected adoptee. If the rearing environment is important, more abnormalities should be observed among the adoptive families of affected than unaffected adoptees (Gottesman and Shields, 1982).
The largest study to use the adoptees family design was the Danish adoption study of schizophrenia (Kety, 1983). This found significantly increased risks of developing DSM-III schizophrenia among biological relatives of suffers than among relatives of the control group. However, there was no increased risk among adopted relatives of affected vs. control (Kety, 1983, Kendler et al, 1984).
The Finish adoption study of schizophrenia (Tienari et al, 1994) confirmed the genetic contribution in schizophrenia;84% of the adopted offspring with schizophrenia developed a non-affective psychotic disorder, compared with only 0.5% of the adopted offspring of control groups (Tienari et al, 1994). However, a gene-environment interaction also emerged in the study (Wahlberg et al, 1997).
When the adoptees were tested for schizophrenia at the mean age of 21, only those adoptees whose biological mother had, had schizophrenia and whose adoptive parents showed high level of communication deviance displayed schizophrenia. This was not observed among adoptees who had only a biological mother with schizophrenia or adoptive parents with a high level of communication deviance (Wahlberg et al, 1997).
Adoption studies confirm the importance of genetic factors in the aetiology of schizophrenia - the Finish adoptive study has provided evidence for gene-environment interaction in the development of schizophrenia.
Psychoanalytic theories have considered disturbed early interaction between parent and child to be an important factor in the development of schizophrenia (Allen, 1976). In the 1946 British cohort study, mothers of children who later developed schizophrenia had worse average general understanding and management of their children, although none of them was known to be mentally ill (Jones, 1983). In the Northern Finish 1966 birth cohort, being a child of an unwanted pregnancy was significantly associated with the later onset of schizophrenia (Myhrman et al, 1996). However, being from a single-parent family was not associated with the risk of developing schizophrenia or other psychotic disorders (Makikyro et al, 1998). Thus, as a result of vast genetic research, family environment has been seen as less and less important. Conversely, the possibility that the childhood rearing environment might be a risk factor for - or a protective force against - the later development of schizophrenia should not be discarded.
Limitations Of The Studies
These studies have divided the opinion of researchers. Some regard the findings as unreliable, caused entirely by the operation of confounding factors, such as narrowing diagnostic criteria; while others believe them to be genuine indicators of the underlying factors affecting the onset of schizophrenia within families. The problem of mechanism of action and interactions of genetic and environmental risk factors is common to all aetiological research on complex diseases (Ottman, 1996).
Limitation 1:Genetic Factors
Twin studies provide evidence of a genetic contribution to schizophrenia: if one identical twin gets the disease, the other has approximately a 30-40% chance of getting it (with a mean delay of 4 years); even if the two have been brought up in different families. Nevertheless, the shared genes of identical twins are not sufficient to give rise to schizophrenia in all instances; i.e. concordance for MZ twins is not 100% and a ‘schizophrenia gene‘ has not been identified despite extensive genome mapping programmes, pointing to the participation of other factors.
Limitation 2:Environmental Factors
People with schizophrenia may display a variety of patterns of aberrant behaviour, raising the possibility that each pattern reflects a different form of the disorder - due to a different cause. However, even MZ twins who both have schizophrenia, and who are presumed to have been afflicted because of shared environmental factors, often have different patterns of symptoms. Therefore, the variability in symptoms does not appear to be a basis for distinguishing between schizophrenia within families due to genetic or environmental causes.
Both genetic and environmental factors have been shown to be important in the aetiology of schizophrenia. Thus, accounting for different aspects of the disorder. However, adopting Gottesman and Shields (1982) combined model of schizophrenia, in which the majority of causes would be attributed to a combined effect of genetic and environmental factors, would seem wise until proved otherwise. Consequently, it can be concluded that genes do not act alone to cause schizophrenia. Environmental factors are also important, although the exact nature of either of their roles is not yet fully established.
- Allen, M. (1976) Archives of General Psychiatry, 33:1476 - 1478. Cited in Gross, R and McIlveen (1998) Psychology: A New Introduction, Hodder & Stoughton.
- Cannon, T.D., Mednick, S.A., Parnas, J. (1998) Archives of General Psychiatry, 47:622-632. Cited in Gleitman, H, Fridlund, A.J. and Reisbery, D. (1998), Psychology, Norton.
- Cardno et al (1999). Cited in Long, P.W. (M.D.) Internet Mental Health (www.mentalhealth.com)
- Gottesman, I.I., Shields, J. (1982) Schizophrenia: The Epigenetic Puzzle. New York: Cambridge University Press. Cited in Gleitman, H, Fridlund, A.J. and Reisbery, D. (1998), Psychology, Norton.
- Jones, R.E. (1983) Hospital Community Psychiatry, 34:807-811. Cited in Gleitman, H, Fridlund, A.J. and Reisbery, D. (1998), Psychology, Norton.
- Kendler, K.S. and Gruenberg, A.M. (1984) Archives of General Psychiatry, 41:555-564. Cited in Gleitman, H, Fridlund, A.J. and Reisbery, D. (1998), Psychology, Norton.
- Kety, S.S. (1983) Journal of American Psychiatry, 140:720-727. Cited in Gleitman, H, Fridlund, A.J. and Reisbery, D. (1998), Psychology, Norton.
- Kringlen and Cramer, D. (1989). Cited in Long, P.W. (M.D.) Internet Mental Health (www.mentalhealth.com).
- Makikyro et al (1998). Cited in Long, P.W. (M.D.) Internet Mental Health (www.mentalhealth.com)
- Myhrman et al (1996). Cited in The Medical Post (1996) Maclean Hunter Publishing Ltd.
- Ottman (1996). Cited in The Medical Post (1996) Maclean Hunter Publishing Ltd.
- Tienari et al (1994) The Finnish Adoption Study Of Schizophrenia. Cited in Gross, R and McIlveen (1998) Psychology: A New Introduction, Hodder & Stoughton.
- Wahlberg et al (1997). Cited in Long P.W. (M.D.) Internet Mental Health (www.mentalhealth.com)
Also used www.schizophrenia.co.uk
Here's what a teacher thought of this essay
In this well-researched account of the contribution made by genes and the environment to the development of schizophrenia, the writer shows clearly how MZ and DZ twin studies have aided our understanding of the role played by these underlying factors. This is an eloquent piece of scientific writing which wastes few words and relies on a wide range of studies carried out in the latter part of the 20th century. If there is any weakness in the essay, it is that the contribution made to the subject by 21st century DNA sequencing technology has been omitted (e.g. Singh and O'Reilly), but overall, this is an impressive piece of writing given the very small word limit.