Evaluation

• DOPAMINE IMBALANCES MAY BE CAUSED BY GENES

  If dopamine imbalances are responsible for schizophrenia, the question then has to be what causes the dopamine imbalances? Many researchers believe that it may be a genetic predisposition, and indeed twin and family studies indicate that there is some genetic basis for schizophrenia.
• DOPAMINE IMBALANCES MAY BE CAUSED BY GENES

  For example, the classic study by Irving Gottesman et al. (1991) looked at the incidence of schizophrenia in cousins, grandchildren, half-siblings, parents, siblings, non-identical and identical twins. As genetic similarity increased so did the probability of both individuals having schizophrenia.
• DOPAMINE IMBALANCES MAY BE CAUSED BY GENES

  However, research looking for one or a few candidate genes has been disappointing. In 2014, the Schizophrenia Working Group of the Psychiatric Genomics Consortium (a group of over 300 scientists from 35 countries) reported that there were 108 genetic loci associated with schizophrenia. This shows that although there may indeed be a genetic basis for schizophrenia, it is a complex matter - more than just a few abnormal dopamine genes.
• MEASURING METABOLITES

  It is not easy to make direct measurements of neurotransmitters such as dopamine, and most of the research that supports the dopamine hypothesis is based on metabolite research. To assess neurotransmitter levels we have to measure the metabolite levels (what neurotransmitters get broken down into) in cerebrospinal fluid.
• MEASURING METABOLITES

  Dopamine becomes metabolised into HVA or homovanillic acid and this is measured in cerebrospinal fluid, which can only be obtained from a lumbar puncture (an unpleasant procedure). 
• MEASURING METABOLITES

  The participants' diet and drug use may also seriously affect metabolite levels and, even when research is conducted under controlled conditions, the results can be difficult to interpret with HVA levels varying widely between participants. 
• MEASURING METABOLITES

  This suggests that until we have refined procedures for measuring neurotransmitters we should perhaps be cautious in the conclusions we draw from metabolite-based research.
• THE ROLE OF SEROTONIN

  Dopamine is not the only neurotransmitter implicated in schizophrenia. Serotonin, another neurotransmitter, has also been identified as a potential influence.
• THE ROLE OF SEROTONIN

  Conventional antipsychotics have traditionally worked by primarily blockading the D2 receptor sites, however not all of those with schizophrenia benefit from these drugs. Newer, atypical antipsychotics such as clozapine, block the D2 receptor and also the serotonin receptor 5-HT2A equally
• THE ROLE OF SEROTONIN

  Although this may not suggest that the dopamine hypothesis is completely wrong, it certainly suggests it cannot explain schizophrenia on its own. This means that, at best, it is only a partial explanation.
• DOPAMINE - CAUSE OR EFFECT?

  Although the dopamine hypothesis proposes that dopamine imbalances cause schizophrenia, it could also legitimately be proposed that schizophrenia causes dopamine imbalances. Are the dopamine discrepancies seen in some people with schizophrenia just another symptom of the disease, rather than a cause of it?
• DOPAMINE - CAUSE OR EFFECT?

  There is some hope that, as Investigative techniques become less invasive, we will be able to conduct research that will be able establish which comes first, a dopamine imbalance or schizophrenia.
• DOPAMINE - CAUSE OR EFFECT?

  Research using PET scans (e.g. Copolov and Crook, 2000) hasn't yet been able to even detect differences in the dopamine activity of the brains of individuals with schizophrenia and those without. So it may be some time before we know for certain if dopamine imbalances cause schizophrenia or if schizophrenia causes dopamine imbalances.
• APPLY THIS EXPLANATION TO MODIFYING SCHIZOPHRENIA: DRUG TREATMENT

  One of the biggest benefits of using neurotransmitters such as dopamine to explain schizophrenia has to be its application to drug treatments. Phenothiazine was the earliest type of antipsychotic drug and it revolutionised psychiatry. It sedates the person and reduces symptoms of schizophrenia such as delusions and hallucinations by binding to dopamine receptors and blocking the build-up of dopamine.
• APPLY THIS EXPLANATION TO MODIFYING SCHIZOPHRENIA: DRUG TREATMENT

  Prior to the introduction of phenothiazines in the 1950s, schizophrenia was generally considered to be untreatable. Apart from incarceration in mental institutions, previous (generally unsuccessful) treatments included insulin shock and ECT - both controversial treatments that involve creating an epileptic fit as a means of shocking the brain into change.
• APPLY THIS EXPLANATION TO MODIFYING SCHIZOPHRENIA: DRUG TREATMENT

  One of the first controlled pieces of research investigating the effectiveness of phenothiazines, reported that 75% of those given the drug were 'much improved' compared with only 25% of those receiving a placebo (Cole et al., 1964). In addition, 48% of those in the placebo condition were considered to have gotten worse compared to none in the phenothiazine condition.