The Dopamine Hypothesis as a Causal Explanation of Schizophrenia

Abstract

Schizophrenia, a severe psychiatric disorder, profoundly impacts individuals, families, and society, characterized by symptoms such as delusions, hallucinations, disorganized thinking, speech, and motor behavior, as outlined in the DSM-5 criteria. Coined by Eugen Bleuler in 1911 to emphasize fragmented cognition, the term "schizophrenia" replaced Emile Kraepelin's "dementia praecox"(1908) reflecting its chronic nature, with an estimated prevalence of 1% in the general population and a significant heritability rate of around 79%. The dopamine hypothesis, central to schizophrenia research, suggests heightened dopaminergic transmission as a primary factor in its development, supported by the efficacy of antipsychotic drugs targeting dopamine receptors. However, recent studies have revealed complexities beyond dopamine dysfunction, including the glutamate hypothesis, which proposes deficits in glutamate activity as an alternative explanation. This essay critically evaluates the dopamine hypothesis within the broader biopsychosocial framework, emphasizing the interaction of biological, psychological, and social factors in schizophrenia etiology. Despite its foundational role, the dopamine hypothesis has limitations in fully clarifying the multifaceted nature of schizophrenia, highlighting the need for comprehensive approaches integrating diverse perspectives and methodologies to enhance understanding of this complex disorder. Keywords: Dopamine Hypothesis, Schizophrenia, Mental Illness, Psychotic Symptoms, GENE x ENVIROMENT Interaction