Schizophrenia is a psychotic disorder (or a group of disorders) marked by severely impaired thinking, emotions, and behaviors. The biological explanations for schizophrenia suggest that it is biological faults with the sufferer that induce schizophrenia. Included is that the condition is a genetic predisposition and is inherited from those who carry the gene, although the phenotype isn’t necessarily expressed. This is already a fault with the theory because this suggests that there must need to be an environmental trigger to set the condition off (therefore not wholly biological). The diathesis-stress model suggests that mental disorders occur when there is a genetic vulnerability, which is triggered by environmental conditions. However, Rabkin (1980) found that schizophrenics didn’t report any significant stressful event before the onset of the condition. However, these self-reports aren’t particularly reliable as the patient may not actually remember (possibly due to repression), want to say or be able to communicate an event which may have triggered it. Gottesman (1991) investigated twin studies of monozygotic and dizygotic twins. He summarized 40 concordance studies and found that when one of the twins was diagnosed with schizophrenia, monozygotic twins showed a 48% concordance rate over a 17% concordance rate in dizygotic twins. Due to the monozygotic twins sharing 100% of their DNA and dizygotic sharing only 50%, this shows that genetics are very likely to play a role in someone developing schizophrenia. However, due to concordance rates not being 100% in MZ twins, it also suggests that some environmental factors must play a role too. Loehlin and Nichols (1976) suggested that the high concordance rates in MZ twins is most likely to be due to the fact they will be treated very similarly from looking the same and living with shared environmental influences. Kendler et al (1995) did a family study and found that 1st degree relatives to someone with schizophrenia were 18 times more likely to be diagnosed with schizophrenia. If there was no genetic element, then there shouldn’t be a difference in the level of risk between 1st degree relatives and a random member of the public (1%). This strongly suggests a link between genetics and the diagnosis of schizophrenia. Neurological explanations of schizophrenia say that if schizophrenia is genetic, then there must be some neurological (brain) differences. Post mortem exams showed that schizophrenic brains are 6% lighter and the cortex was found with fewer neurons. However, with these post mortems, there is no way of establishing a cause and effect. It could be that these brain differences caused the schizophrenia, or the schizophrenia caused the brain differences. Similarly, PET and CAT scans found that schizophrenics tended to have larger ventricles and a small frontal cortex. They also found brain cell loss in the temporal lobes (linked with cognition and emotion), which has been associated with negative symptoms (an absence of behaviour). Again these findings are only a correlation and with symptoms like enlarged ventricles, non-schizophrenics have been found with them too. However, this may not be due to an absence of the schizophrenic gene, but more to do with the fact these people have not been faced with a trigger for the condition. The sample sizes of the people undergoing these brain scans are also very small which means the results cannot really be generalised and may be more down to chance. Harrison (1995) suggested that the neurological differences may be due to anoxia at birth (lack of oxygen e.g. umbilical cord wrapped around the babies neck) and that these birth complications could be what triggers the brain differences rather than genetics. Biological explanations also look into biochemistry and the influence of dopamine (a neurotransmitter). It has been found that drugs