Schizophrenia is a complex psychiatric disorder involving genetic, neurobiological, and environmental factors. While no single cause exists, certain drugs can act as triggers, particularly in genetically vulnerable individuals.

Strong Evidence for Triggering Role:

• Cannabis (THC): High-potency cannabis use, especially in adolescence, doubles the risk of schizophrenia onset. A 2019 Lancet Psychiatry meta-analysis of 10 studies (n=66,000) found daily high-THC users had 3–5x higher odds. THC disrupts dopamine signaling and brain maturation during critical windows (ages 12–25).
• Stimulants (Amphetamines, Cocaine): These induce transient psychosis in ~40% of heavy users; 10–20% progress to chronic schizophrenia-like illness. A 2021 JAMA Psychiatry study (n=6,700) showed methamphetamine users had 4.5x risk if family history present.
• Hallucinogens (LSD, Psilocybin): Rare but documented; can unmask latent vulnerability via serotonin dysregulation.

Mechanism: Drugs hijack dopamine/serotonin pathways already dysregulated in predisposed brains. Twin studies show 50% heritability; drugs lower the threshold for symptom emergence.

Not Causation Alone: Most drug users never develop schizophrenia (~1% population risk). Protective factors include later onset, low genetic load, and social support. A 2023 Nature Reviews Neuroscience paper emphasizes gene-environment interaction: DRD2/COMT variants + substance use = synergistic risk.

Key Caveats:

• Correlation ≠ causation; reverse causality possible (prodromal symptoms drive drug use).
• Prescription drugs (e.g., steroids, anticholinergics) rarely implicated.
• Alcohol/nicotine linked to worse prognosis but not primary triggers.

Clinical Implications: Screen at-risk youth (family history, early psychosis signs) for substance use. Early intervention (CBT, antipsychotics) prevents progression in 30–50% of drug-induced cases.

In summary: Drugs like cannabis and stimulants can precipitate schizophrenia in vulnerable individuals but do not cause it de novo. Risk is dose-dependent and genetically moderated. Prevention focuses on delaying adolescent exposure and monitoring high-risk groups.