Schizophrenia is a complex mental disorder affecting about 1% of the global population, characterized by hallucinations, delusions, disorganized thinking, and impaired functioning. No single cause exists; it arises from a interplay of genetic, biological, environmental, and neurochemical factors. Understanding these helps reduce stigma and guide treatment.

Genetic Factors: Schizophrenia has a strong hereditary component. Twin studies show concordance rates of 40-50% in identical twins versus 10-15% in fraternal twins. Over 100 genetic loci are linked, including variants in genes like COMT and DISC1, which affect brain development. If a parent has schizophrenia, a child's risk rises to 10-15%; with both parents, it reaches 40%. However, genetics alone don't cause it most people with risk genes never develop the disorder.

Neurobiological Factors: Brain imaging reveals structural abnormalities, such as enlarged ventricles, reduced gray matter in the prefrontal cortex and hippocampus, and disrupted white matter connectivity. Neurodevelopmental issues, like prenatal insults (e.g., maternal infections or malnutrition), may alter brain wiring. Dopamine dysregulation is central: the "dopamine hypothesis" posits excess dopamine in mesolimbic pathways causes positive symptoms (hallucinations), while deficits in mesocortical pathways lead to negative symptoms (apathy). Glutamate imbalance, via NMDA receptor hypofunction, also contributes.

Environmental Triggers: Stressful life events, urban upbringing, migration, and childhood trauma increase risk by 2-3 times. Prenatal exposures famine, viral infections (e.g., influenza), or obstetric complications raise odds. Cannabis use, especially high-potency strains in adolescence, doubles risk in vulnerable individuals by disrupting endocannabinoid signaling.

Interaction Model: The diathesis-stress model explains onset: genetic vulnerability (diathesis) interacts with environmental stressors to trigger symptoms, often in late adolescence/early adulthood. Epigenetic changes, like DNA methylation from trauma, can "switch on" risk genes.

While causes are multifactorial and not fully elucidated, early intervention targeting modifiable risks (e.g., substance avoidance) is key. Research continues via GWAS and neuroimaging