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• One of the major strengths of the dopamine hypothesis is that it is biologically based, making it more scientific and testable than purely psychological explanations. Evidence from drug research supports the idea that increased dopamine activity is linked to psychotic symptoms. For example, amphetamines, which increase dopamine levels, can induce schizophrenia-like symptoms in healthy individuals, while antipsychotic medications, which block dopamine receptors (particularly D2 receptors), often reduce positive symptoms such as hallucinations and delusions. This provides empirical support and has led to real-life applications in the form of pharmacological treatments for schizophrenia, significantly improving the quality of life for many patients.
• Despite its strengths, the dopamine hypothesis has several limitations. Firstly, it is often criticized for being too reductionist, as it focuses primarily on one neurotransmitter and ignores the complex interplay of genetic, environmental, and social factors that may contribute to schizophrenia. For instance, it fails to account for negative symptoms (such as flat affect or social withdrawal), which are often less responsive to dopamine-blocking medications
• A key criticism of the dopamine hypothesis is that it promotes biological determinism, the idea that behavior and mental disorders are entirely controlled by biological factors, such as genes or neurotransmitters. This perspective can be problematic, as it implies that individuals with schizophrenia have little to no control over their condition, which may lead to pessimism about recovery and a reliance on medication as the sole form of treatment
• An important criticism of the dopamine hypothesis comes from David Healy (2002), who argues that the theory may have been heavily influenced by the pharmaceutical industry. Healy suggests that drug companies have deliberately exaggerated the role of dopamine in schizophrenia to promote the widespread use of antipsychotic medications. By presenting an overly simplistic explanation—that schizophrenia is caused by excessive dopamine activity—it becomes much easier to market antipsychotic drugs as the most effective, or even only, treatment option
• This raises concerns about scientific objectivity, as research may be skewed by financial interests rather than a genuine pursuit of understanding. The dominance of this narrative could have led to the neglect of alternative explanations and treatments, such as psychological therapies or social interventions, which may be equally or more beneficial, especially for managing negative symptoms or improving long-term functioning
• : Research suggests that dopamine may play a key role in schizophrenic symptomatology e.g.  et al. (1999), Desbonnet (2016) with brain-imaging studies demonstrating high activity in dopamine-rich areas of the brains of schizophrenics.
• There may, however, also be other neurotransmitters involved in schizophrenia: Grunder & Cumming (2016) point out that the dopamine hypothesis should be modified to include the role of glutamate as a key contributory factor in promoting schizophrenic symptoms.