Antipsychotic drugs and diabetes- : an application of the Austin Bradford Hill criteria

There is concern that antipsychotic drugs cause diabetes. Although there has been an explosion in the quantity of literature about this subject, it remains confusing and inconsistent. To assess whether the association between antipsychotic drugs and diabetes is causative, we applied the Austin Bradf...

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Bibliographic Details
Published in:Diabetologia 2006-07, Vol.49 (7), p.1467-1476
Main Authors: HOLT, R. I. G, PEVELER, R. C
Format: Article
Language:English
Subjects:
Antipsychotic Agents - adverse effects
Antipsychotics
Biological and medical sciences
Case reports
Cohort analysis
Cross-sectional studies
Diabetes
Diabetes Mellitus - chemically induced
Diabetes. Impaired glucose tolerance
Diabetic Neuropathies - complications
Diabetic Neuropathies - etiology
Drugs
Endocrine pancreas. Apud cells (diseases)
Endocrinopathies
Etiopathogenesis. Screening. Investigations. Target tissue resistance
Family medical history
Humans
Medical sciences
Models, Theoretical
Neuropharmacology
Pharmacology. Drug treatments
Psychiatrists
Psycholeptics: tranquillizer, neuroleptic
Psychology. Psychoanalysis. Psychiatry
Psychopharmacology
Psychotropic drugs
Risk Factors
Schizophrenia - complications
Schizophrenia - drug therapy
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Summary:There is concern that antipsychotic drugs cause diabetes. Although there has been an explosion in the quantity of literature about this subject, it remains confusing and inconsistent. To assess whether the association between antipsychotic drugs and diabetes is causative, we applied the Austin Bradford Hill criteria to the available evidence. In support of a causative relationship, there is temporality for some cases of diabetes, and there is a biologically plausible explanation. The causative link between antipsychotic drugs and diabetes is coherent with our understanding of diabetes and there are other analogies. However the strength of association is weak, there is lack of consistency or specificity, and there is little evidence to support a biological gradient. We should therefore conclude that the evidence surrounding a causative link between antipsychotic drugs and diabetes is inconclusive. Moreover, the risk is probably low and the attributable risk of developing diabetes is greater for traditional risk factors such as family history, ethnicity, obesity and ageing than it is for receiving an antipsychotic drug. Consequently, the majority of patients receiving second-generation antipsychotics will not develop diabetes as a result of their medication.
ISSN:0012-186X
1432-0428
DOI:10.1007/s00125-006-0279-3