Cannabis and Anhedonia in Psychiatric Disorders: A Systematic Review

Background: Cannabis use is common among individuals with psychiatric disorders, but its relationship with anhedonia and reward-processing deficits remains unclear. Anhedonia is multidimensional, encompassing anticipatory and consummatory pleasure, motivation, reward learning, and neurobiological signatures such as blunted striatal dopamine release and reduced reward-related activation in mesocorticolimbic regions. THC, the primary psychoactive constituent of cannabis, acts directly on CB1 receptors within this circuitry. However, findings on how THC-specific cannabis use affects anhedonia and reward-related outcomes across psychiatric populations are inconsistent, varying by dose, frequency, and use pattern. This systematic review synthesizes current literature on THC-specific cannabis use and anhedonia or reward-related outcomes across psychiatric disorders. Methods: Following PRISMA 2020 guidelines, Medline, PsycINFO, and Embase were searched through March 2026. Eligible studies included experimental, quasi-experimental, and observational designs assessing cannabis exposure in populations with clinical or subclinical psychiatric disorders or symptoms, reporting at least one subjective, behavioral, or neurobiological measure of anhedonia or reward processing (e.g., anticipatory/consummatory pleasure, effort-based motivation, reward responsiveness, or neural reward activity). Results: Twenty studies met inclusion criteria, spanning psychosis-spectrum disorders (13 studies, N = 53,043), MDD/depressive symptoms (8 studies, N = 4,657), bipolar disorder (1 study, N = 103), and anxiety symptoms (1 study, N = 153). In schizophrenia and first-episode psychosis, longitudinal studies consistently linked cannabis use to reduced intrinsic motivation and blunted neural reward sensitivity, while cross-sectional findings were mixed. Among clinical high-risk youth, cannabis use was inversely associated with baseline social anhedonia but did not predict subsequent change. In MDD, cannabis use disorder—rather than general use—predicted greater odds of anhedonia onset over 3–6-year follow-up; five of seven moderate-to-high-quality studies found significant associations. Abstinence/treatment findings were mixed: a 28-day abstinence paradigm reduced self-reported anhedonia, while reduced cannabis use during CBT/MET was linked to reduced ventral striatal reward activation despite depressive symptom improvement. The bipolar study found no association with physical anhedonia; the anxiety study found greater cannabis severity linked to anticipatory but not consummatory anhedonia. Conclusions: Evidence most consistently implicates CUD in worsening motivational and anticipatory reward deficits in schizophrenia and MDD. Findings for bipolar and anxiety disorders are limited. Methodological heterogeneity underscores the need for longitudinal, mechanistic studies clarifying causal pathways and disorder-specific vulnerabilities.