EXPLANATION 1: DOPAMINE HYPOTHESIS-EVALUATION AO3 Flashcards
SUPPORTING EVIDENCE:
TIMMONS AND HAMILTON
EVIDENCE COMES FROM THE FACT THAT AMPHETAMINE INCREASES THE AMOUNT OF DOPAMINE. TIMMONS AND HAMILTON REPORTED THAT HIGH DOSES OF AMPHETAMINE (A DRUG WHICH STIMULATES DA ACTIVITY) CAN RESULT IN AN ACUTE PSYCHOSIS RESEMBLING SCHIZOPHRENIA IN CLINICALLY NORMAL PEOPLE
SUPPORTING EVIDENCE:
GJEDDE AND WONG
THEY FOUND THAT SCHIZOPHRENICS HAVE MORE THAN TWICE AS MANY DOPAMINE RECEPTORS THAN CONTROLS (CLINICALLY NORMAL PEOPLE)
SUPPORTING EVIDENCE:
IVERSEN
HE REPORTED THAT POST-MORTEMS ON SCHIZOPHRENICS FOUND EXCESSIVE DOPAMINE IN THE LIMBIC SYSTEM SUGGESTING THAT THE NEUROTRANSMITTER IS INVOLVED IN THE DISORDER
SUPPORTING EVIDENCE:
BARLOW AND DURAND
THE DEVELOPMENT OF ANTIPSYCHOTICS PROVIDES SUPPORT FOR THE DOPAMINE EXPLANATIONS. BARLOW AND DURAND REPORT THAT CHLOROPROMAZINE IS EFFECTIVE IN REDUCING SCHIZOPHRENIC SYMPTOMS IN ABOUT 60% OF CASES-THIS WORKS BY BLOCKING DOPAMINE RECEPTORS, SO PREVENTING DOPAMINE-RECEIVING NEURONS FROM FIRING, REDUCING DOPAMINE LEVELS
WEAKENING EVIDENCE:
DAVIS ET AL
HE REPORTED THAT HIGH LEVELS OF DOPAMINE ARE NOT FOUND IN ALL SCHIZOPHRENICS, AND THE MODERN ANTI-SCHIZOPHRENIC DRUG CLOZAPINE, WITH VERY LITTLE DOPAMINE BLOCKING ACTIVITY, WORKS EFFECTIVELY AGAINST THE DISORDER
WEAKENING EVIDENCE:
THE EXCESSIVE DOPAMINE EXPLANATION DOES NOT EXPLAIN WHETHER THE EXCESS DOPAMINE ACTIVITY WAS RESPONSIBLE FOR THE POSITIVE SYMPTOMS, NEGATIVE SYMPTOMS, OR BOTH. DRUGS DIDN’T WORK FOR INDIVIDUALS WHO HAD NEGATIVE SYMPTOMS.
METHODOLOGICAL ISSUES:
(METABOLITE RESEARCH)
There are also methodological issues with the dopamine hypothesis. For example, it is challenging to make direct measurements of neurotransmitters such as dopamine. Instead, researchers often rely on metabolite levels such as homovanillic acid in cerebrospinal fluid as an indirect indicator of dopamine activity. This reliance on indirect measures means that they aren’t capturing the exact levels of dopamine, but rather what it gets broken down into, which may not fully reflect dopamine activity in the brain.
METHODOLOGICAL ISSUES:
(CAUSE AND EFFECT?)
Although the dopamine hypothesis proposes that dopamine imbalances cause schizophrenia, it could also legitimately be proposed that schizophrenia causes the dopamine imbalances. Are the dopamine discrepancies seen in some people with schizophrenia just another symptom of the disease, rather than a cause of it? There is some hope that, as investigative techniques become less invasive, we will be able to conduct research that will be able to establish which comes first, a dopamine imbalance or schizophrenia.
METHODOLOGICAL ISSUES:
(COPOLOV AND CROOK/PET SCANS)
Research using PET scans (e.g., Copolov & 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 causes dopamine imbalances.
METHODOLOGICAL ISSUES:
Dopamine is not the only neurotransmitter implicated in schizophrenia. Serotonin, another neurotransmitter, has also been identified as a potential influence. 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 the serotonin receptor 5-HT2A equally. 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.
REDUCTIONIST:
Another issue with the dopamine hypothesis is that it is reductionist. This means that it is over simplifying our understanding of this complex behaviour down to just one or two factors (dopamine and dopamine receptor sites). This weakens the dopamine hypothesis as it ignores other biological factors, such as brain abnormalities, environmental factors such as dysfunctional family communication and cognitive disorders that could cause schizophrenia
DETERMINISTIC:
The dopamine hypothesis is also a biologically deterministic explanation. This is because it suggests that excess dopamine will always cause schizophrenia. Whilst this might not always be the case, if the overwhelming evidence supports this, then we can develop effective treatments that reduces dopamine levels, which allows patients to lead normal lives with their families.
