We cannot base our opinions on concordance rates because they suggest that there are other factors that influence schizophrenia, therefore it can be considered quite vague. Most twins also share very similar environments than siblings so this must also be taken into account.
Particularly for early studies, sophisticated genetic testing was very difficult to distinguish MZ and DZ twins, especially at birth. Some of the statistics for MZ twins may actually be DZ twins and vice versa.
We tend to assume that MZ twins are treated more alike because they are MZ twins. Lytton (1977) turned this on its head and suggested that the greater similarity of MZ twins ensures that they elicit a more similar response from their parents. That is the greater similarity of identical twins is a cause of their more similar parenting rather than an effect of it.
Adoptee studies have found good support for the genetic theory for schizophrenia. Heston (1966) studied adopted away offspring of schizophrenic mothers and found a significant rate of schizophrenia in these children (10.4% prevalence, which became 16.6% when necessary age corrections were made). Children from unaffected mothers showed no symptoms of schizophrenia.
While it may be easier to distinguish between genetic and environmental factors in adoption studies, because the adopted child is raised away from the genetic parent and environment, adoption studies are very difficult to carry out. This is because the necessary information about parent and child is rarely available. In the cases where it is available there may have been contact between the child and the genetic parent, making it more difficult to distinguish between genetic and environmental influence.
A genetic predetermination could lead to abnormalities in the brain. Weinberger and Wyatt (1982) conducted research into schizophrenia by examining CAT scans and the ventricle size of the brain. It appears that the ventricles in the lower half of the brain are larger in schizophrenics compared to that of ‘normal’ individuals.
However, it is impossible to make a categorical link as some have argued that increased ventricle size is linked to natural processes that occur at or before birth.
Suddath (1990) constructed a study to investigate discordant twin pairs for structural abnormalities that might account for the incidence of schizophrenia in one of each pair. His method involved fifteen discordant monozygotic twin pairs, only one of which was diagnosed with schizophrenia. The twins were given MRI scans to determine any differences in brain structures between the twins in each discordant pair.
The results showed that the co-twin with schizophrenia had a smaller bilateral hippocampus than the twin without schizophrenia in 14 out of 15 of the pairs. The co-twin with schizophrenia had larger ventricles. This concludes that when genotype is controlled for, there is significantly diminished brain volume in the twin with schizophrenia. However it is difficult to establish whether the smaller hippocampus found in the schizophrenic twins is a cause of effect of the schizophrenia.
However, Harrison (1995) believes that these differences occur before the onset of schizophrenia, implying that they are more likely to be a cause than an outcome of the disorder. Since the abnormalities in brain structure do not increase over time, as is the case with diseases like Alzheimer’s, then it appears that the problems are due to a failure of the brain to develop normally in the first place.
One criticism often aimed at the possible relationship between brain damage and schizophrenia, is that no one pattern of damage seems to correlate with the disorder. It seems that certain damage is associated with certain symptoms however; damage to the temporal lobe is associated with some of the positive symptoms whereas damage to the frontal lobe is associated more with the negative symptoms.
Any such differences between the brain of a ‘schizophrenic’ and ‘non-schizophrenic’ brain are so small that it is not possible to detect them in the individual. They only become apparent if groups of schizophrenics and non-schizophrenics are compared.