Schizophrenia has been suggested as a syndrome of accelerated aging. Telomere length (TL) decrease is considered one biological marker associated with age and can be accelerated by pathological characteristics present in schizophrenia. Several studies evaluated TL in schizophrenia, but the results are still controversial. The aim of this study was to conduct a meta-analysis of the existing results of TL in leukocytes of individuals with schizophrenia compared to healthy controls. A search was performed in PubMed, using the keywords 'telomere schizophrenia' and 'telomere psychosis'. We included data from original articles that measured TL in leukocytes of human patients with schizophrenia and healthy control subjects. 45 articles were found, but only 7 met our criteria. Telomere length of controls was not statistically different from that of patients with schizophrenia (p=0.07). Crossvalidation with the leave-one-out method resulted in a significant model (p=0.03) in which TL of individuals with schizophrenia is smaller than control (SMD=0.38; 95% CI=[0.05, 0.72]). We also propose a biological pathway through which schizophrenia could promote telomere erosion and how antipsychotics might compensate this loss. There are few studies made on this subject with diverse methodology and heterogeneous sample. Some articles did not consider other possible influences on TL. Overall our results suggest that TL is decreased in schizophrenia. Although this is consistent with the idea of accelerated aging, schizophrenia is a complex disease and there are several factors that influence TL that should be controlled in future studies.