Introduction The prevalence of diabetes in schizophrenia is twice that in the general population, but there are few reliable predictors of which individuals will develop glucose dysregulation.
Objective To test if abnormal birth weight (either too low or too high) and parental diabetes, both variables that can be ascertained in the clinic, can predict diabetes onset in patients with schizophrenia.
Research design and methods Electronic records of a cohort of 190 clozapine-treated patients (37% treated for more than 20 years) and Cox regression survival analysis (with any type of glucose dysregulation as the event) to account for differences in length of treatment before the event and age at clozapine treatment initiation.
Results Age at clozapine initiation (Exp(B)=1.098; p<0.001), family history of diabetes (Exp(B)=2.299; p=0.049) and birth weight2 (Exp(B)=0.999; p=0.013) were significant predictors of glucose dysregulation onset, while gender was not (Exp(B)=0.1.350; p=0.517). Among individuals with 10 years of follow-up, 80% of those with both abnormal birth weight and a family history of diabetes developed diabetes compared with 56% with only abnormal birth weight, 40% with only a family history of diabetes and 20% in those with neither.
Conclusions Since 48% of cases had at least one risk factor and 6% had both risk factors, there is a substantial proportion of patients for whom preventive strategies could be implemented.
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Contributors EF-E, RW and HZ conceptualized and designed the project. EF-E and RW collected the data. EF-E, HZ, RNC and ETB designed the analyses, and EF-E conducted the analyses. EF-E and HZ wrote the first draft, which was edited and commented by ETB, RNC and RW. All authors approved the final manuscript. EF-E is the guarantor of this work, and as such had full access to all the data in the study and takes responsibility for the integrity of the data and the accuracy of the data analysis.
Funding EF-E and the research database were supported by intramural funding from CPFT and the UK National Institute for Health Research (NIHR) Cambridge Biomedical Research Centre (BRC); the views expressed are those of the authors and not necessarily those of the NIHR or the Department of Health and Social Care. RNC’s research is supported by the UK Medical Research Council (MC_PC_17213).
Competing interests None declared.
Patient consent for publication Not required.
Ethics approval Data were collected as part of an ethically approved database for research and clinical purposes (‘Clinical and Research Database in Persistent Schizophrenia’; NHS Research Ethics reference (NRES) 13/EE/0121).
Provenance and peer review Not commissioned; externally peer reviewed.
Data availability statement Data are available upon reasonable request.
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